Updated on 2025/07/10

写真a

 
KAWASAKI Katsushige
 
Organization
Academic Assembly Institute of Medicine and Dentistry SHIGAKU KEIRETU Assistant Professor
Graduate School of Medical and Dental Sciences Oral Life Science Assistant Professor
Title
Assistant Professor
External link

Degree

  • 博士（歯学） ( 2009.3   新潟大学 )

Research Areas

  • Life Science / Developmental dentistry

  • Life Science / Oral biological science

Research History (researchmap)

  • Niigata University   Graduate School of Medical and Dental Sciences   Assistant Professor

    2015.4

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  • Niigata University   Graduate School of Medical and Dental Sciences

    2015.3

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  • Niigata University   Medical and Dental Hospital

    2013.11 - 2015.2

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  • King's College London UK   Craniofacial Development & Stem Cell Biology   Research Fellow(新潟大学医歯学総合研究科:組織的な若手研究者等海外派遣プログラム）

    2011.1 - 2013.10

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  • Niigata University   Medical and Dental Hospital

    2008.4 - 2010.12

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Research History

  • Niigata University   Graduate School of Medical and Dental Sciences Oral Life Science   Assistant Professor

    2015.4

  • Niigata University   Graduate School of Medical and Dental Sciences   Specially Appointed Assistant Professor

    2015.3

 

Papers

  • A Novel KDF1 Variant is Associated With Multiple Natal Teeth, Tooth Agenesis, and Root Maldevelopment. International journal

    John M Graham Jr, Pedro A Sanchez-Lara, Atsushi Ohazama, Katsushige Kawasaki, Stefan T Arold, Piranit Nik Kantaputra

    International dental journal   75 ( 4 )   100860 - 100860   2025.6

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    Language：English   Publishing type：Research paper (scientific journal)  

    OBJECTIVE: Natal teeth are teeth that are present at birth. Multiple natal teeth are extremely rare. The objective of this study was to find the molecular aetiology of a unique dental phenotype including natal teeth, tooth agenesis, and root maldevelopment in a 5-generation family. METHODS: Oral and radiographic examination, linkage analysis, whole genome sequencing, and an immunohistochemical study of Kdf1 during tooth development in the mouse embryo were performed. A protein model was generated. RESULTS: We report a 5-generation family in which multiple natal teeth, oligodontia, and root maldevelopment manifested with autosomal dominant inheritance. Linkage analysis and whole genome sequencing revealed a novel pathogenic variant c.845T>G; p.Ile282Ser, which cosegregated in 9 affected and 10 unaffected family members. This amino acid Ile282 is highly conserved and is important for the stabilization of a small helical fragment. This stabilization is lost in the Ile282Ser mutant, resulting in disruption of the interaction of KDF1 with its partner proteins, including IKKA, which are important for epidermal proliferation and differentiation and subsequent tooth development. CONCLUSIONS: Our study demonstrates for the first time that natal teeth, tooth agenesis, and root maldevelopment are caused by a KDF1 variant. Our study highlights the important role of KDF1 in tooth formation and eruption.

    DOI： 10.1016/j.identj.2025.100860

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  • Heimler Syndrome With Tooth Agenesis, Abnormal Enamel and Dentin Mineralization, Root Maldevelopment, and PEX1 Mutation. International journal

    Piranit N Kantaputra, Atitaya Apivatthakakul, Massupa Kaewgahya, Sissades Tongsima, Chumpol Ngamphiw, Thanapat Sastraruji, Panwarit Sukantamala, Bruce M Carlson, Katsushige Kawasaki, James R Ketudat Cairns, Nuntigar Sonsuwan, Atsushi Ohazama

    International dental journal   75 ( 4 )   100821 - 100821   2025.6

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    Biallelic variants in the PEX1 and PEX6 genes are implicated in Heimler syndrome, which is characterized by amelogenesis imperfecta, sensorineural hearing loss, retinitis pigmentosa, and nail defects. The objective of this study is to find the genetic variant and to analyze the teeth of a patient with Heimler syndrome. Clinical and radiographic examination and whole exome sequencing were performed on a Heimler syndrome patient and his parents. Scanning electron microscopy and micro-computed tomography were performed on a tooth. Immunohistochemical study of Pex1 was performed. Mutant protein models were made. The authors report an 18-year-old male with Heimler syndrome who carried a compound heterozygous (c.2966T>C; p.Ile989Thr and c.2097_2098insT; p.Ile700TyrfsTer42) mutation in the PEX1 gene. Clinical manifestations included amelogenesis imperfecta of the posterior permanent teeth, mild sensorineural hearing loss, retinitis pigmentosa, and leukonychia. SEM showed enamel and dentin dysmineralization. The newly findings include arachnodactyly, tooth agenesis, microdontia, root maldevelopment, and failure of tooth eruption. The p.Ile700TyrfsTer42 variant is predicted to produce a non-viable protein. The p.Ile989Thr variant is predicted to disrupt its interaction with PEX6. A patient with Heimler syndrome may have arachnodactyly, tooth agenesis, microdontia, delayed dental development, root maldevelopment, enamel and dentin dysmineralization, and failure of tooth eruption.

    DOI： 10.1016/j.identj.2025.04.002

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  • DNA repair during embryonic epidermal stratification. International journal

    Fumiya Meguro, Katsushige Kawasaki, Yoshito Kakihara, Maiko Kawasaki, Makoto Fukushima, Finsa Tisna Sari, Vanessa Utama, Alex Kesuma, Jun Nihara, Takehisa Kudo, Akira Fujita, Kaya Ichikawa, Kazuaki Osawa, Takeyasu Maeda, Koichi Tabeta, Makio Saeki, Atsushi Ohazama

    Developmental dynamics : an official publication of the American Association of Anatomists   2025.5

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    BACKGROUND: Genomes are constantly exposed to a myriad of DNA-damaging agents. Robust DNA repair mechanisms protect DNA by removing or tolerating damage. However, it remains unclear whether these mechanisms are required for organogenesis. RESULTS: Multiple epithelial layers are essential for skin function, including body protection. The epidermis is initiated as a single layer and then stratifies in utero. Stratification did not occur in mice with epithelial conditional deletion of the DNA repair molecule Reptin (Reptinfl/fl;K14Cre). DNA damage was observed in the mutant epidermis but not in the wild-type epidermis. The mutant epidermis also showed reduced cell proliferation and upregulated p53 expression. Stratification was restored when p53 was deleted in the Reptin mutant mice by generating Reptin and p53 double mutant mice (Reptinfl/fl;K14Cre;p53-/-). CONCLUSION: In the wild-type epidermis, DNA is likely damaged at the initiation of embryonic stratification and promptly repaired by DNA repair mechanisms involving Reptin.

    DOI： 10.1002/dvdy.70046

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  • Cell-cell interaction determines cell fate of mesoderm-derived cell in tongue development through Hh signaling. International journal

    Maiko Kawasaki, Katsushige Kawasaki, Finsa Tisna Sari, Takehisa Kudo, Jun Nihara, Madoka Kitamura, Takahiro Nagai, Vanessa Utama, Yoko Ishida, Fumiya Meguro, Alex Kesuma, Akira Fujita, Takayuki Nishimura, Yuan Kogure, Satoshi Maruyama, Jun-Ichi Tanuma, Yoshito Kakihara, Takeyasu Maeda, Sarah Ghafoor, Roman H Khonsari, Pierre Corre, Paul T Sharpe, Martyn Cobourne, Brunella Franco, Atsushi Ohazama

    eLife   13   2024.10

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    Dysfunction of primary cilia leads to genetic disorder, ciliopathies, which shows various malformations in many vital organs such as brain. Multiple tongue deformities including cleft, hamartoma, and ankyloglossia are also seen in ciliopathies, which yield difficulties in fundamental functions such as mastication and vocalization. Here, we found these tongue anomalies in mice with mutation of ciliary protein. Abnormal cranial neural crest-derived cells (CNCC) failed to evoke Hh signal for differentiation of mesoderm-derived cells into myoblasts, which resulted in abnormal differentiation of mesoderm-derived cells into adipocytes. The ectopic adipose subsequently arrested tongue swelling formation. Ankyloglossia was caused by aberrant cell migration due to lack of non-canonical Wnt signaling. In addition to ciliopathies, these tongue anomalies are often observed as non-familial condition in human. We found that these tongue deformities could be reproduced in wild-type mice by simple mechanical manipulations to disturb cellular processes which were disrupted in mutant mice. Our results provide hints for possible future treatment in ciliopathies.

    DOI： 10.7554/eLife.85042

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  • Homozygosity for a Rare Plec Variant Suggests a Contributory Role in Congenital Insensitivity to Pain. International journal

    Piranit Kantaputra, Teerada Daroontum, Kantapong Kitiyamas, Panat Piyakhunakorn, Katsushige Kawasaki, Achara Sathienkijkanchai, Pornswan Wasant, Nithiwat Vatanavicharn, Thippawan Yasanga, Massupa Kaewgahya, Sissades Tongsima, Timothy C Cox, Stefan T Arold, Atsushi Ohazama, Chumpol Ngamphiw

    International journal of molecular sciences   25 ( 12 )   2024.6

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    Congenital insensitivity to pain is a rare human condition in which affected individuals do not experience pain throughout their lives. This study aimed to identify the molecular etiology of congenital insensitivity to pain in two Thai patients. Clinical, radiographic, histopathologic, immunohistochemical, and molecular studies were performed. Patients were found to have congenital insensitivity to pain, self-mutilation, acro-osteolysis, cornea scars, reduced temperature sensation, tooth agenesis, root maldevelopment, and underdeveloped maxilla and mandible. The skin biopsies revealed fewer axons, decreased vimentin expression, and absent neurofilament expression, indicating lack of dermal nerves. Whole exome and Sanger sequencing identified a rare homozygous variant c.4039C>T; p.Arg1347Cys in the plakin domain of Plec, a cytolinker protein. This p.Arg1347Cys variant is in the spectrin repeat 9 region of the plakin domain, a region not previously found to harbor pathogenic missense variants in other plectinopathies. The substitution with a cysteine is expected to decrease the stability of the spectrin repeat 9 unit of the plakin domain. Whole mount in situ hybridization and an immunohistochemical study suggested that Plec is important for the development of maxilla and mandible, cornea, and distal phalanges. Additionally, the presence of dental anomalies in these patients further supports the potential involvement of Plec in tooth development. This is the first report showing the association between the Plec variant and congenital insensitivity to pain in humans.

    DOI： 10.3390/ijms25126358

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  • Genetic Variants in KCTD1 Are Associated with Isolated Dental Anomalies. International journal

    Cholaporn Ruangchan, Chumpol Ngamphiw, Annop Krasaesin, Narin Intarak, Sissades Tongsima, Massupa Kaewgahya, Katsushige Kawasaki, Phitsanu Mahawong, Kullaya Paripurana, Bussaneeya Sookawat, Peeranat Jatooratthawichot, Timothy C Cox, Atsushi Ohazama, James R Ketudat Cairns, Thantrira Porntaveetus, Piranit Kantaputra

    International journal of molecular sciences   25 ( 10 )   2024.5

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    KCTD1 plays crucial roles in regulating both the SHH and WNT/β-catenin signaling pathways, which are essential for tooth development. The objective of this study was to investigate if genetic variants in KCTD1 might also be associated with isolated dental anomalies. We clinically and radiographically investigated 362 patients affected with isolated dental anomalies. Whole exome sequencing identified two unrelated families with rare (p.Arg241Gln) or novel (p.Pro243Ser) variants in KCTD1. The variants segregated with the dental anomalies in all nine patients from the two families. Clinical findings of the patients included taurodontism, unseparated roots, long roots, tooth agenesis, a supernumerary tooth, torus palatinus, and torus mandibularis. The role of Kctd1 in root development is supported by our immunohistochemical study showing high expression of Kctd1 in Hertwig epithelial root sheath. The KCTD1 variants in our patients are the first variants found to be located in the C-terminal domain, which might disrupt protein-protein interactions and/or SUMOylation and subsequently result in aberrant WNT-SHH-BMP signaling and isolated dental anomalies. Functional studies on the p.Arg241Gln variant are consistent with an impact on β-catenin levels and canonical WNT signaling. This is the first report of the association of KCTD1 variants and isolated dental anomalies.

    DOI： 10.3390/ijms25105179

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  • CACNA1S mutation-associated dental anomalies: A calcium channelopathy. International journal

    P Kantaputra, A Butali, S Eliason, C Chalkley, S Nakornchai, C Bongkochwilawan, K Kawasaki, A Kumchiang, C Ngamphiw, S Tongsima, J R Ketudat Cairns, B Olsen, W Intachai, A Ohazama, A S Tucker, B A Amendt

    Oral diseases   30 ( 3 )   1350 - 1359   2024.4

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    OBJECTIVES: To identify the molecular etiology of distinct dental anomalies found in eight Thai patients and explore the mutational effects on cellular functions. MATERIALS AND METHODS: Clinical and radiographic examinations were performed for eight patients. Whole exome sequencing, mutant protein modelling, qPCR, western blot analysis, scratch assays, immunofluorescence, confocal analysis, in situ hybridization, and scanning electron micrography of teeth were done. RESULTS: All patients had molars with multiple supernumerary cusps, single-cusped premolars, and a reduction in root number. Mutation analysis highlighted a heterozygous c.865A>G; p.Ile289Val mutation in CACNA1S in the patients. CACNA1S is a component of the slowly inactivating L-type voltage-dependent calcium channel. Mutant protein modeling suggested that the mutation might allow leakage of Ca2+ or other cations, or a tightening, to restrict calcium flow. Immunohistochemistry analysis showed expression of Cacna1s in the developing murine tooth epithelium during stages of crown and root morphogenesis. In cell culture, the mutation resulted in abnormal cell migration of transfected CHO cells compared to wildtype CACNA1S, with changes to the cytoskeleton and markers of focal adhesion. CONCLUSIONS: The malformations observed in our patients suggest a role for calcium signaling in organization of both cusps and roots, affecting cell dynamics within the dental epithelium.

    DOI： 10.1111/odi.14551

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  • Physiological analyses of swallowing changes due to chronic obstructive pulmonary disease in anesthetized male rats. International journal

    Kouta Nagoya, Takanori Tsujimura, Midori Yoshihara, Masahiro Watanabe, Jin Magara, Katsushige Kawasaki, Makoto Inoue

    Frontiers in physiology   15   1445336 - 1445336   2024

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    Chronic obstructive pulmonary disease (COPD) was previously known as chronic bronchitis and emphysema. It has various main symptoms, such as dyspnea, chronic cough, and sputum, and is often accompanied by dysphagia. Although many published clinical reports have described COPD-related dysphagia, the physiological mechanisms underlying swallowing changes due to COPD remain unclear. Therefore, we analyzed how COPD affects the swallowing reflex using COPD model rats. We performed an electrophysiological study of respiration and swallowing using COPD model induced by intratracheal administration of porcine pancreatic elastase and lipopolysaccharide in Sprague-Dawley male rats. To identify the respiration and swallowing responses, electromyographic activity was recorded from the diaphragm, digastric (Dig), and thyrohyoid (TH) muscles. We confirmed COPD using micro-computed tomography analysis and hematoxylin and eosin staining of the lungs. The duty cycle was defined as the ratio of the inspiration duration to the total respiratory duration. In COPD model rats, the duty cycle was significantly higher than that in control rats. The frequency of the swallowing reflex evoked by electrical stimulation of the superior laryngeal nerve during the inspiration phase was higher in COPD model rats than in control rats. Furthermore, long-term COPD altered Dig and TH muscle activity without pathological muscle change. Our results suggest that COPD increases the frequency of swallowing initiation during the inspiration phase. Furthermore, long-term COPD affects swallowing-related muscle activity without pathological muscle changes. These physiological changes may increase the risk of developing dysphagia. Further studies are necessary to clarify the mechanisms contributing to the functional changes in respiration and swallowing in COPD.

    DOI： 10.3389/fphys.2024.1445336

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  • Ift88 regulates enamel formation via involving Shh signaling. Reviewed International journal

    Takehisa Kudo, Maiko Kawasaki, Katsushige Kawasaki, Fumiya Meguro, Jun Nihara, Izumi Honda, Madoka Kitamura, Akira Fujita, Kazuaki Osawa, Kaya Ichikawa, Takahiro Nagai, Yoko Ishida, Paul T Sharpe, Takeyasu Maeda, Isao Saito, Atsushi Ohazama

    Oral diseases   29 ( 4 )   1622 - 1631   2023.5

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    DOI： 10.1111/odi.14162

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    Other Link： https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20K10092/

  • A Mutation in CACNA1S Is Associated with Multiple Supernumerary Cusps and Root Maldevelopment. International journal

    Piranit Kantaputra, Niramol Leelaadisorn, Athiwat Hatsadaloi, Natalina Quarto, Worrachet Intachai, Sissades Tongsima, Katsushige Kawasaki, Atsushi Ohazama, Chumpol Ngamphiw, Paswach Wiriyakijja

    Diagnostics (Basel, Switzerland)   13 ( 5 )   2023.2

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    BACKGROUND: Enamel knots and Hertwig epithelial root sheath (HERS) regulate the growth and folding of the dental epithelium, which subsequently determines the final form of tooth crown and roots. We would like to investigate the genetic etiology of seven patients affected with unique clinical manifestations, including multiple supernumerary cusps, single prominent premolars, and single-rooted molars. METHODS: Oral and radiographic examination and whole-exome or Sanger sequencing were performed in seven patients. Immunohistochemical study during early tooth development in mice was performed. RESULTS: A heterozygous variant (c. 865A>G; p.Ile289Val) in CACNA1S was identified in all the patients, but not in an unaffected family member and control. Immunohistochemical study showed high expression of Cacna1s in the secondary enamel knot. CONCLUSIONS: This CACNA1S variant seemed to cause impaired dental epithelial folding; too much folding in the molars and less folding in the premolars; and delayed folding (invagination) of HERS, which resulted in single-rooted molars or taurodontism. Our observation suggests that the mutation in CACNA1S might disrupt calcium influx, resulting in impaired dental epithelium folding, and subsequent abnormal crown and root morphology.

    DOI： 10.3390/diagnostics13050895

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  • A novel P3H1 mutation is associated with osteogenesis imperfecta type VIII and dental anomalies. International journal

    Piranit Nik Kantaputra, Prapai Dejkhamron, Worrachet Intachai, Chumpol Ngamphiw, James R Ketudat Cairns, Katsushige Kawasaki, Atsushi Ohazama, Bjorn Olsen, Sissades Tongsima, Salita Angkurawaranon

    Oral surgery, oral medicine, oral pathology and oral radiology   132 ( 6 )   e198-e207 - 4564   2021.12

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    OBJECTIVE: Our objective was to investigate the molecular etiology of osteogenesis imperfecta type VIII and dental anomalies in 4 siblings of a Karen tribe family. MATERIALS AND METHODS: Four patients and their unaffected parents were studied by clinical and radiographic examination. In situ hybridization of P3h1 during early murine tooth development, whole-exome sequencing, and Sanger direct sequencing were performed. RESULTS: A novel homozygous missense P3H1 mutation (NM_001243246.1; c.2141A>G; NP_001230175.1; p.Lys714Arg) was identified in all patients. Their unaffected parents were heterozygous for the mutation. The mutation is hypothesized to belong to isoform c of P3H1. Mutations in P3H1 are associated with autosomal recessive osteogenesis imperfecta type VIII. Hypodontia, a mesiodens, and single-rooted permanent second molars found in our patients have never been reported in patients with P3H1 mutations. Single-rooted second permanent molars or failure to form multiple roots implies effects of the P3H1 mutation on root development. CONCLUSIONS: We report a novel P3H1 mutation as the underlying cause of osteogenesis imperfecta type VIII with dental anomalies. Our study suggests that isoform c of P3H1 is also a functional isoform of P3H1. We report, for the first time, to our knowledge, the association of P3H1 mutation and osteogenesis imperfecta type VIII with dental anomalies.

    DOI： 10.1016/j.oooo.2021.01.023

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  • Expression of R-spondins/Lgrs in development of movable craniofacial organs. International journal

    Jun Nihara, Maiko Kawasaki, Katsushige Kawasaki, Akane Yamada, Fumiya Meguro, Takehisa Kudo, Supaluk Trakanant, Takahiro Nagai, Isao Saito, Takeyasu Maeda, Atsushi Ohazama

    Gene expression patterns : GEP   41   119195 - 119195   2021.9

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    DOI： 10.1016/j.gep.2021.119195

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  • MicroRNAs regulate distal region of mandibular development through Hh signaling. International journal

    Supaluk Trakanant, Jun Nihara, Takahiro Nagai, Maiko Kawasaki, Katsushige Kawasaki, Yoko Ishida, Fumiya Meguro, Takehisa Kudo, Akane Yamada, Takeyasu Maeda, Isao Saito, Atsushi Ohazama

    Journal of anatomy   238 ( 3 )   711 - 719   2021.3

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    DOI： 10.1111/joa.13328

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  • Overactivation of the NF-kappa B pathway impairs molar enamel formation Reviewed International journal

    Akane Yamada, Maiko Kawasaki, Yasuo Miake, Yurie Yamada, James Blackburn, Katsushige Kawasaki, Supaluk Trakanant, Takahiro Nagai, Jun Nihara, Takehisa Kudo, Fumiya Meguro, Ruth Schmidt-Ullrich, Bigang Liu, Yinling Hu, Angustias Page, Angel Ramirez, Paul T. Sharpe, Takeyasu Maeda, Ritsuo Takagi, Atsushi Ohazama

    ORAL DISEASES   26 ( 7 )   1513 - 1522   2020.10

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    DOI： 10.1111/odi.13384

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  • Changes in signalling pathways in the palatal cleft in CL/Fr mice Reviewed

    Akane Yamada, Takahiro Nagai, Atsushi Kitamura, Maiko Kawasaki, Katsushige Kawasaki, Yasumitsu Kodama, Takeyasu Maeda, Atsushi Ohazama, Ritsuo Takagi

    JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY MEDICINE AND PATHOLOGY   32 ( 5 )   331 - 335   2020.9

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    DOI： 10.1016/j.ajoms.2019.12.001

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  • Clouston syndrome with pili canaliculi, pili torti, overgrown hyponychium, onycholysis, taurodontism and absence of palmoplantar keratoderma. Reviewed International journal

    Piranit Kantaputra, Worrachet Intachai, Katsushige Kawasaki, Atsushi Ohazama, Bruce Carlson, Natalina Quarto, Chulabhorn Pruksachatkun, Mati Chuamanochan

    The Journal of dermatology   47 ( 6 )   e230-e232   2020.6

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  • Juberg-Hayward syndrome is a cohesinopathy, caused by mutation in ESCO2. Reviewed International journal

    Piranit Nik Kantaputra, Prapai Dejkhamron, Worrachet Intachai, Chumpol Ngamphiw, Katsushige Kawasaki, Atsushi Ohazama, Suttichai Krisanaprakornkit, Bjorn Olsen, Sissades Tongsima, Jame R Ketudat Cairns

    European journal of orthodontics   43 ( 1 )   45 - 50   2020.4

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    BACKGROUND: Juberg-Hayward syndrome (JHS; MIM 216100) is a rare autosomal recessive malformation syndrome, characterized by cleft lip/palate, microcephaly, ptosis, short stature, hypoplasia or aplasia of thumbs, and dislocation of radial head and fusion of humerus and radius leading to elbow restriction. OBJECTIVE: To report for the first time the molecular aetiology of JHS. PATIENT AND METHODS: Clinical and radiographic examination, whole exome sequencing, Sanger sequencing, mutant protein model construction, and in situ hybridization of Esco2 expression in mouse embryos were performed. RESULTS: Clinical findings of the patient consisted of repaired cleft lip/palate, microcephaly, ptosis, short stature, delayed bone age, hypoplastic fingers and thumbs, clinodactyly of the fifth fingers, and humeroradial synostosis leading to elbow restriction. Intelligence is normal. Whole exome sequencing of the whole family showed a novel homozygous base substitution c.1654C>T in ESCO2 of the proband. The sister was homozygous for the wildtype variant. Parents were heterozygous for the mutation. The mutation is predicted to cause premature stop codon p.Arg552Ter. Mutations in ESCO2, a gene involved in cohesin complex formation, are known to cause Roberts/SC phocomelia syndrome. Roberts/SC phocomelia syndrome and JHS share similar clinical findings, including autosomal recessive inheritance, short stature, cleft lip/palate, severe upper limb anomalies, and hypoplastic digits. Esco2 expression during the early development of lip, palate, eyelid, digits, upper limb, and lower limb and truncated protein model are consistent with the defect. CONCLUSIONS: Our study showed that Roberts/SC phocomelia syndrome and JHS are allelic and distinct entities. This is the first report demonstrating that mutation in ESCO2 causes JHS, a cohesinopathy.

    DOI： 10.1093/ejo/cjaa023

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  • Molecular mechanisms in palatal rugae development Reviewed International journal

    Supaluk Trakanant, Jun Nihara, Maiko Kawasaki, Fumiya Meguro, Akane Yamada, Katsushige Kawasaki, Isao Saito, Maeda Takeyasu, Atsushi Ohazama

    JOURNAL OF ORAL BIOSCIENCES   62 ( 1 )   30 - 35   2020.3

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    DOI： 10.1016/j.job.2019.12.002

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  • Ift88 is involved in mandibular development Reviewed International journal

    Atsushi Kitamura, Maiko Kawasaki, Katsushige Kawasaki, Fumiya Meguro, Akane Yamada, Takahiro Nagai, Yasumitsu Kodama, Supaluk Trakanant, Paul T. Sharpe, Takeyasu Maeda, Ritsuo Takagi, Atsushi Ohazama

    JOURNAL OF ANATOMY   236 ( 2 )   317 - 324   2020.2

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    DOI： 10.1111/joa.13096

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  • Primary cilia in murine palatal rugae development Reviewed International journal

    Mayuko Nakaniwa, Maiko Kawasaki, Katsushige Kawasaki, Akane Yamada, Fumiya Meguro, Maeda Takeyasu, Atsushi Ohazama

    GENE EXPRESSION PATTERNS   34   119062 - 119062   2019.12

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    DOI： 10.1016/j.gep.2019.119062

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  • Bmp signaling in molar cusp formation Reviewed International journal

    Fumiya Meguro, Thantrira Porntaveetus, Maiko Kawasaki, Katsushige Kawasaki, Akane Yamada, Yoshito Kakihara, Makio Saeki, Koichi Tabeta, John A. Kessler, Takeyasu Maeda, Atsushi Ohazama

    GENE EXPRESSION PATTERNS   32   67 - 71   2019.6

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    DOI： 10.1016/j.gep.2019.04.002

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  • Ift88 limits bone formation in maxillary process through suppressing apoptosis Reviewed International journal

    Momoko Watanabe, Maiko Kawasaki, Katsushige Kawasaki, Atsushi Kitamura, Takahiro Nagai, Yasumitsu Kodama, Fumiya Meguro, Akane Yamadaa, Paul T. Sharpe, Takeyasu Maeda, Ritsuo Takagi, Atsushi Ohazama

    ARCHIVES OF ORAL BIOLOGY   101   43 - 50   2019.5

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    DOI： 10.1016/j.archoralbio.2019.02.017

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  • ADAMTSL1 and mandibular prognathism. Reviewed International journal

    Piranit N Kantaputra, Apitchaya Pruksametanan, Nattapol Phondee, Athiwat Hutsadaloi, Worrachet Intachai, Katsushig Kawasaki, Atsushi Ohazama, Chumpol Ngamphiw, Sissades Tongsima, James R Ketudat Cairns, Polbhat Tripuwabhrut

    Clinical genetics   95 ( 4 )   507 - 515   2019.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    Mandibular prognathism is characterized by a prognathic or prominent mandible. The objective of this study was to find the gene responsible for mandibular prognathism. Whole exome sequencing analysis of a Thai family (family 1) identified the ADAMTSL1 c.176C>A variant as the potential defect. We cross-checked our exome data of 215 people for rare variants in ADAMTSL1 and found that the c.670C>G variant was associated with mandibular prognathism in families 2 and 4. Mutation analysis of ADAMTSL1 in 79 unrelated patients revealed the c.670C>G variant was also found in family 3. We hypothesize that mutations in ADAMTSL1 cause failure to cleave aggrecan in the condylar cartilage, and that leads to overgrowth of the mandible. Adamtsl1 is strongly expressed in the condensed mesenchymal cells of the mouse condyle, but not at the cartilage of the long bones. This explains why the patients with ADAMTSL1 mutations had abnormal mandibles but normal long bones. This is the first report that mutations in ADAMTSL1 are responsible for the pathogenesis of mandibular prognathism.

    DOI： 10.1111/cge.13519

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  • MicroRNAs control eyelid development through regulating Wnt signaling Reviewed International journal

    Takahiro Nagai, Supaluk Trakanant, Maiko Kawasaki, Katsushige Kawasaki, Yurie Yamada, Momoko Watanabe, James Blackburn, Yoko Otsuka-Tanaka, Mitsue Hishinuma, Atsushi Kitatmura, Fumiya Meguro, Akane Yamada, Yasumitsu Kodama, Takeyasu Maeda, Qiliang Zhou, Yasuo Saijo, Akihiro Yasue, Paul T. Sharpe, Robert Hindges, Ritsuo Takagi, Atsushi Ohazama

    DEVELOPMENTAL DYNAMICS   248 ( 3 )   201 - 210   2019.3

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    DOI： 10.1002/dvdy.10

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  • Lrp4/Wise regulates palatal rugae development through Turing-type reaction-diffusion mechanisms Reviewed International journal

    Maiko Kawasaki, Katsushige Kawasaki, Fumiya Meguro, Akane Yamada, Ryuichi Ishikawa, Thantrira Porntaveetus, James Blackburn, Yoko Otsuka-Tanaka, Naoaki Saito, Masato S. Ota, Paul T. Sharpe, John A. Kessler, Joachim Herz, Martyn T. Cobourne, Takeyasu Maeda, Atsushi Ohazama

    PLOS ONE   13 ( 9 )   e0204126   2018.9

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    DOI： 10.1371/journal.pone.0204126

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  • Expanding the Oro-Dental and Mutational Spectra of Kabuki Syndrome and Expression of KMT2D and KDM6A in Human Tooth Germs Reviewed International journal

    Thantrira Porntaveetus, Mushriq F. Abid, Thanakorn Theerapanon, Chalurmpon Srichomthong, Atsushi Ohazama, Katsushige Kawasaki, Maiko Kawasaki, Kanya Suphapeetiporn, Paul T. Sharpe, Vorasuk Shotelersuk

    INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES   14 ( 4 )   381 - 389   2018

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    DOI： 10.7150/ijbs.23517

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  • Sox Genes Show Spatiotemporal Expression during Murine Tongue and Eyelid Development. Reviewed International journal

    Ryuichi Ishikawa, Maiko Kawasaki, Katsushige Kawasaki, Akane Yamada, Supaluk Trakanant, Fumiya Meguro, Atsushi Kitamura, Takehisa Kudo, Takeyasu Maeda, Atsushi Ohazama

    International journal of dentistry   2018   1601363 - 1601363   2018

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    The tongue is a critical organ, involved in functions such as speaking, swallowing, mastication, and degustation. Although Sox genes are known to play critical roles in many biological processes, including organogenesis, the expression of the Sox family members during tongue development remains unclear. We therefore performed a comparative in situ hybridization analysis of 17 Sox genes (Sox1-14, 17, 18, and 21) during murine tongue development. Sox2, 4, 6, 8, 9, 10, 11, 12, and 21 were found to be expressed in the tongue epithelium, whereas Sox2, 4-6, 8-11, 13, and 21 showed expression in the mesenchyme of the developing tongue. Expression of Sox1, 4, 6, 8-12, and 21 were observed in the developing tongue muscle. Sox5 and 13 showed expression only at E12, while Sox1 expression was observed only on E18. Sox6, 8, 9, and 12 showed expression at several stages. Although the expression of Sox2, 4, 10, 11, and 21 was detected during all the four stages of tongue development, their expression patterns differed among the stages. We thus identified a dynamic spatiotemporal expression pattern of the Sox genes during murine tongue development. To understand whether Sox genes are involved in the development of other craniofacial organs through similar roles to those in tongue development, we also examined the expression of Sox genes in eyelid primordia, which also contain epithelium, mesenchyme, and muscle. However, expression patterns and timing of Sox genes differed between tongue and eyelid development. Sox genes are thus related to organogenesis through different functions in each craniofacial organ.

    DOI： 10.1155/2018/1601363

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  • Al-Awadi-Raas-Rothschild syndrome with dental anomalies and a novel WNT7A mutation. Reviewed International journal

    Piranit Nik Kantaputra, Seema Kapoor, Prashant Verma, Massupa Kaewgahya, Katsushige Kawasaki, Atsushi Ohazama, James R Ketudat Cairns

    European journal of medical genetics   60 ( 12 )   695 - 700   2017.12

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    DOI： 10.1016/j.ejmg.2017.09.005

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  • TFAP2B mutation and dental anomalies. Reviewed International journal

    Natchaya Tanasubsinn, Rekwan Sittiwangkul, Yupada Pongprot, Katsushige Kawasaki, Atsushi Ohazama, Thanapat Sastraruji, Massupa Kaewgahya, Piranit Nik Kantaputra

    Journal of human genetics   62 ( 8 )   769 - 775   2017.8

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    DOI： 10.1038/jhg.2017.37

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  • Regional Regulation of Filiform Tongue Papillae Development by Ikk alpha/Irf6 Reviewed International journal

    Maiko Kawasaki, Katsushige Kawasaki, Shelly Oommen, James Blackburn, Momoko Watanabe, Takahiro Nagai, Atsushi Kitamura, Takeyasu Maeda, Bigang Liu, Ruth Schmidt-Ullrich, Taishin Akiyama, Jun-Ichiro Inoue, Nigel L. Hammond, Paul T. Sharpe, Atsushi Ohazama

    DEVELOPMENTAL DYNAMICS   245 ( 9 )   937 - 946   2016.9

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    DOI： 10.1002/DVDY.24427

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  • Spatio-temporal expression of Sox genes in murine palatogenesis Reviewed International journal

    Momoko Watanabe, Katsushige Kawasaki, Maiko Kawasaki, Thantrira Portaveetus, Shelly Oommen, James Blackburn, Takahiro Nagai, Atsushi Kitamura, Atsushi Nishikawa, Yasumitsu Kodama, Ritsuo Takagi, Takeyasu Maeda, Paul T. Sharpe, Atsushi Ohazama

    GENE EXPRESSION PATTERNS   21 ( 2 )   111 - 118   2016.7

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    DOI： 10.1016/j.gep.2016.05.002

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  • GREMLIN 2 Mutations and Dental Anomalies Reviewed

    P. N. Kantaputra, M. Kaewgahya, A. Hatsadaloi, P. Vogel, K. Kawasaki, A. Ohazama, J. R. Ketudat Cairns

    JOURNAL OF DENTAL RESEARCH   94 ( 12 )   1646 - 1652   2015.12

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    DOI： 10.1177/0022034515608168

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  • Excess NF-kappa B Induces Ectopic Odontogenesis in Embryonic Incisor Epithelium Reviewed

    J. Blackburn, K. Kawasaki, T. Porntaveetus, M. Kawasaki, Y. Otsuka-Tanaka, Y. Miake, M. S. Ota, M. Watanabe, M. Hishinuma, T. Nomoto, S. Oommen, S. Ghafoor, F. Harada, K. Nozawa-Inoue, T. Maeda, R. Peterkova, H. Lesot, J. Inoue, T. Akiyama, R. Schmidt-Ullrich, B. Liu, Y. Hu, A. Page, A. Ramirez, P. T. Sharpe, A. Ohazama

    JOURNAL OF DENTAL RESEARCH   94 ( 1 )   121 - 128   2015.1

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1177/0022034514556707

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  • Expression of Sox genes in tooth development Reviewed International journal

    Katsushige Kawasaki, Maiko Kawasaki, Momoko Watanabe, Erik Idrus, Takahiro Nagai, Shelly Oommen, Takeyasu Maeda, Nobuko Hagiwara, Jianwen Que, Paul T. Sharpe, Atsushi Ohazama

    INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY   59 ( 10-12 )   471 - 478   2015

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1387/ijdb.150192ao

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  • R-spondins/Lgrs expression in tooth development Reviewed International journal

    Maiko Kawasaki, Thantrira Porntaveetus, Katsushige Kawasaki, Shelly Oommen, Yoko Otsuka-Tanaka, Mitsue Hishinuma, Takato Nomoto, Takeyasu Maeda, Keiyo Takubo, Toshio Suda, Paul T. Sharpe, Atsushi Ohazama

    DEVELOPMENTAL DYNAMICS   243 ( 6 )   844 - 851   2014.6

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1002/dvdy.24124

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  • PKA regulatory subunit expression in tooth development. Reviewed International journal

    Sílvia Ferreira de Sousa, Katsushige Kawasaki, Maiko Kawasaki, Ana Angelova Volponi, Ricardo Santiago Gomez, Carolina Cavaliéri Gomes, Paul T Sharpe, Atsushi Ohazama

    Gene expression patterns : GEP   15 ( 1 )   46 - 51   2014.5

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    DOI： 10.1016/j.gep.2014.04.002

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  • Tooth brushing for oral prophylaxis Reviewed

    Haruaki Hayasaki, Issei Saitoh, Kuniko Nakakura-Ohshima, Mika Hanasaki, Yukiko Nogami, Tsutomu Nakajima, Emi Inada, Tomonori Iwasaki, Yoko Iwase, Tadashi Sawami, Katsushige Kawasaki, Nozomi Murakami, Tomoya Murakami, Mie Kurosawa, Masami Kimi, Akiko Kagoshima, Miki Soda, Youich Yamasaki

    Japanese Dental Science Review   50 ( 3 )   69 - 77   2014

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier Ltd  

    DOI： 10.1016/j.jdsr.2014.04.001

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  • Multiple postnatal craniofacial anomalies are characterized by conditional loss of polycystic kidney disease 2 (Pkd2) Reviewed

    Roman H. Khonsari, Atsushi Ohazama, Ramin Raouf, Maiko Kawasaki, Katsushige Kawasaki, Thantrira Porntaveetus, Sarah Ghafoor, Peter Hammond, Michael Suttie, Guillaume A. Odri, Richard N. Sandford, John N. Wood, Paul T. Sharpe

    HUMAN MOLECULAR GENETICS   22 ( 9 )   1873 - 1885   2013.5

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    DOI： 10.1093/hmg/ddt041

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  • Oral lining mucosa development depends on mesenchymal microRNAs Reviewed

    Y. Otsuka-Tanaka, S. Oommen, M. Kawasaki, K. Kawasaki, N. Imam, F. Jalani-Ghazani, R. Hindges, P. T. Sharpe, A. Ohazama

    Journal of Dental Research   92 ( 3 )   229 - 234   2013.3

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    DOI： 10.1177/0022034512470830

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  • Distinct roles of MicroRNAs in epithelium and mesenchyme during tooth development Reviewed

    Shelly Oommen, Yoko Otsuka-Tanaka, Najam Imam, Maiko Kawasaki, Katsushige Kawasaki, Farnoosh Jalani-Ghazani, Angela Anderegg, Rajeshwar Awatramani, Robert Hindges, Paul T. Sharpe, Atsushi Ohazama

    DEVELOPMENTAL DYNAMICS   241 ( 9 )   1465 - 1472   2012.9

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    DOI： 10.1002/dvdy.23828

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  • Cytoplasmic Plaque Formation in Hemidesmosome Development Is Dependent on SoxF Transcription Factor Function Reviewed

    Shelly Oommen, Mathias Francois, Maiko Kawasaki, Melanie Murrell, Katsushige Kawasaki, Thantrira Porntaveetus, Sarah Ghafoor, Neville J. Young, Yoshimasa Okamatsu, John McGrath, Peter Koopman, Paul T. Sharpe, Atsushi Ohazama

    PLOS ONE   7 ( 9 )   e43857   2012.9

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    DOI： 10.1371/journal.pone.0043857

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  • Bmp signalling in filiform tongue papillae development Reviewed

    Katsushige Kawasaki, Thantrira Porntaveetus, Shelly Oommen, Sarah Ghafoor, Maiko Kawasaki, Yoko Otsuka-Tanaka, James Blackburn, John A. Kessler, Paul T. Sharpe, Atsushi Ohazama

    ARCHIVES OF ORAL BIOLOGY   57 ( 6 )   805 - 813   2012.6

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    DOI： 10.1016/j.archoralbio.2011.11.014

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  • The role of Irf6 in tooth epithelial invagination Reviewed

    James Blackburn, Atsushi Ohazama, Katsushige Kawasaki, Yoko Otsuka-Tanaka, Bigang Liu, Kenya Honda, Ryan B. Rountree, Yinling Hu, Maiko Kawasaki, Walter Birchmeier, Ruth Schmidt-Ullrich, Akira Kinoshita, Brian C. Schutte, Nigel L. Hammond, Michael J. Dixon, Paul T. Sharpe

    DEVELOPMENTAL BIOLOGY   365 ( 1 )   61 - 70   2012.5

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    DOI： 10.1016/j.ydbio.2012.02.009

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  • A Comparative Study of Masticatory Parameters for School-lunch Intake

    KOBAYASHI Hideki, MATSUYAMA Junko, MITOMI Tomoe, SANO Tomiko, KAWASAKI Katsushige, TAGUCHI Yo

    The Japanese Journal of Pediatric Dentistry   48 ( 3 )   388 - 396   2010.6

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    Language：Japanese   Publisher：Japanese Society of Pediatric Dentistry  

    DOI： 10.11411/jspd.48.3_388

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    Other Link： http://search.jamas.or.jp/link/ui/2010286113

  • Cross-sectional analysis of age-related changes in the fluctuation of bite size Reviewed

    Katsushige Kawasaki, Junko Matsuyama, Yo Taguchi, Tomoe Mitomi

    pediatric dental journal   20 ( 1 )   22 - 27   2010

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    DOI： 10.11411/pdj.20.22

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Books

  • Innovative Research on Biosis-Abiosis Intelligent Interface

    Kawasaki M, Kawasaki K, Blackburn J, Ohazama A（ Role： Joint translator）

    Springer  2017 

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    https://www.springer.com/gp/book/9789811015595

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Presentations

  • 下顎発生における一次繊毛の機能について

    北村 厚, 川崎 勝盛, 川崎 真依子, 児玉 泰光, 前田 健康, 高木 律男, 大峡 淳

    新潟歯学会雑誌  2017.12 

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  • Ofd1は口蓋突起の下方伸長に必須である

    渡部 桃子, 川崎 勝盛, 川崎 真依子, 永井 孝宏, 北村 厚, 児玉 泰光, 前田 健康, 高木 律男, 大峡 淳

    新潟歯学会雑誌  2016.12 

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  • 間葉のMicroRNAは、眼瞼発生を制御する

    永井 孝宏, 渡部 桃子, 川崎 真依子, 川崎 勝盛, 北村 厚, 児玉 泰光, 高木 律男, 前田 健康, 大峡 淳

    新潟歯学会雑誌  2016.12 

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  • Evidence Based Dentistry in Pediatric Dentistry 乳歯用既成冠

    大島 邦子, 三富 智恵, 河野 承子, 飯沢 二葉子, 川崎 勝盛, 早崎 治明

    小児歯科学雑誌  2011.3 

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  • 小児の前歯部交換期における一口量に関する研究

    竹内 優美子, 松山 順子, 川崎 勝盛, 三富 智恵, 佐野 富子, 田口 洋

    新潟歯学会雑誌  2010.12 

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  • 学校給食による咀嚼パラメーターの比較検討 麺類、米飯類、パン類の相違点について

    小林 英樹, 松山 順子, 三富 智恵, 佐野 富子, 川崎 勝盛, 田口 洋

    小児歯科学雑誌  2010.6 

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  • 学校給食に関する咀嚼の検討 麺類、米飯類、パン類の違い

    小林 英樹, 田口 洋, 松山 順子, 三富 智恵, 佐野 富子, 川崎 勝盛

    小児歯科学雑誌  2010.3 

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  • 小児の一口量と前歯部萠出状態との関連性

    竹内 優美子, 松山 順子, 川崎 勝盛, 三富 智恵, 佐野 富子, 田口 洋

    新潟歯学会雑誌  2009.12 

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  • 学校給食による咀嚼パラメーターの比較検討

    小林 英樹, 田口 洋, 松山 順子, 三富 智恵, 佐野 富子, 川崎 勝盛

    新潟歯学会雑誌  2009.12 

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  • The study of growth changes in the mouthful weights and its coefficient variations

    Kawasaki Katsushige

    新潟歯学会雑誌  2009.6 

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  • 食物の取り込みに対する視覚遮断の影響

    川崎 勝盛, 松山 順子, 三富 智恵, 佐野 優美子, 田口 洋

    小児歯科学雑誌  2009.3 

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  • 摂食嚥下機能の発達 一口量の識別能は思春期初期に成熟する

    川崎 勝盛, 松山 順子, 三富 智恵, 佐野 富子, 田口 洋

    日本歯科医師会雑誌  2008.8 

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  • 年齢による食べ方の変化(第2報) 食べ方の成熟に関する横断的研究

    川崎 勝盛, 松山 順子, 三富 智恵, 田口 洋

    小児歯科学雑誌  2008.3 

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  • 小児における成長に伴う一口量の変化の分析 横断的および縦断的研究

    川崎 勝盛, 松山 順子, 三富 恵, 佐野 富子, 田口 洋

    新潟歯学会雑誌  2007.12 

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  • 小児の成長発育に伴う食べ方の成熟に関する研究 一口量に関する分析

    川崎 勝盛, 松山 順子, 三富 智恵, 田口 洋, 野田 忠

    小児歯科学雑誌  2007.5 

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  • 下口唇にみられたFibroepithelial polypの一症例

    川崎 勝盛, 三富 智恵, 野田 忠

    小児歯科学雑誌  2006 

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  • ウサギにおける嚥下誘発性の生後発達について

    小林 博昭, 木島 寛, 梶井 友佳, 川崎 勝盛, 福島 伸一, 田口 洋

    小児歯科学雑誌  2005 

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Research Projects

  • Studying for the role of primary cilium length in tooth development

    Grant number：25K13048

    2025.4 - 2028.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

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    Grant amount：\4680000 （ Direct Cost: \3600000 、 Indirect Cost：\1080000 ）

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  • Investigation for X-inactivation in palate formation

    Grant number：23K18354

    2023.6 - 2025.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Challenging Research (Exploratory)

    Awarding organization：Japan Society for the Promotion of Science

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    Grant amount：\6500000 （ Direct Cost: \5000000 、 Indirect Cost：\1500000 ）

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  • 歯の形成におけるDNA損傷/修復のメカニズムの解明

    Grant number：23K09434

    2023.4 - 2026.3

    System name：科学研究費助成事業

    Research category：基盤研究(C)

    Awarding organization：日本学術振興会

    川崎 真依子, 大峡 淳, 川崎 勝盛

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    Grant amount：\4810000 （ Direct Cost: \3700000 、 Indirect Cost：\1110000 ）

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  • Study for investigating mechanisms of mandibular development

    Grant number：21K10088

    2021.4 - 2024.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

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    Grant amount：\4160000 （ Direct Cost: \3200000 、 Indirect Cost：\960000 ）

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  • Study for investigating mechanisms of mesiodens formation

    Grant number：21K10182

    2021.4 - 2024.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

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    Grant amount：\4160000 （ Direct Cost: \3200000 、 Indirect Cost：\960000 ）

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  • Elucidating the function of primary cilia during maxillofacial development: In terms of signal pathway crosstalk

    Grant number：20K10092

    2020.4 - 2023.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    Kawasaki Maiko

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    Grant amount：\4420000 （ Direct Cost: \3400000 、 Indirect Cost：\1020000 ）

    In this study, the interaction between SHH and WNT signaling pathways was analyzed using morphological and molecular biological techniques in transgenic mice in which both SHH and WNT signaling pathways functioning within the primary cilia were regulated. This revealed the function of primary cilia during the development of the maxillofacial region. Transgenic mice in which both SHH and WNT were regulated showed cleft palate, abnormal tooth number, abnormal tooth morphology, and delayed tooth formation. However, their phenotypes approximated either phenotype of mice in which each was controlled alone. The phenotypes of the mice created by this study were extremely severe morphological abnormalities in the maxillofacial region, indicating that the SHH and WNT signaling pathways each play a very important role as regulators of morphogenesis of the maxillofacial region.

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  • Trail toward development of new treatment for ameloblastoma by intentional cell differentiation

    Grant number：18K19639

    2018.6 - 2021.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Challenging Research (Exploratory)

    Awarding organization：Japan Society for the Promotion of Science

    MAEDA TAKEYASU

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    Grant type：Competitive

    Grant amount：\6370000 （ Direct Cost: \4900000 、 Indirect Cost：\1470000 ）

    At post-maturation stage in normal tooth development, ameloblasts differentiate into reduced enamel epithelial cells which exhibit low biological activity. These reduced enamel epithelial cells are fallen out during tooth eruption. It is believed that ameloblastoma is caused by tumorigenesis of enamel forming cells. It is possible that ameloblastoma become harmless when ameloblastoma differentiate into reduced enamel epithelial cells. However, the molecular mechanisms inducing reduced enamel epithelial cells are remained unclear. We found that reduced enamel epithelium decreased their biological activity by activating senescence.

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  • analysis of the comprehensive molecular mechanism of temporomandibular joint formation

    Grant number：18K09762

    2018.4 - 2021.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    kawasaki katsushige

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\4420000 （ Direct Cost: \3400000 、 Indirect Cost：\1020000 ）

    Abnormalities of temporomandibular joint are seldom occurred in mice with targeted gene mutation. Therefore, the molecular mechanisms of temporomandibular joint formation remain unclear. We generated mice with mesenchymal deletions of the ciliary protein, Ift88 (Ift88fl/fl;Wnt1Cre), and found aberrant temporomandibular joint. The abnormal temporomandibular joint was found to be caused by aberrant mandibular formation. In Ift88fl/fl;Wnt1Cre mice, downregulation of Hh signaling led to the abnormal mandibular formation, which induced aberrant temporomandibular joint formation.

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  • Study of the involvement of epigenetics in cleft palate

    Grant number：17K11954

    2017.4 - 2020.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    ISHIDA Yoko

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    Grant type：Competitive

    Grant amount：\4550000 （ Direct Cost: \3500000 、 Indirect Cost：\1050000 ）

    Non - syndromic cleft lip with or without cleft palate is one of the most common birth defects in humans. Dicer plays a critical role in the biogenesis of multiple classes of small RNAs. We generated mesenchyme-specific mutations of Dicer using the Cre/loxP-recombination system, and analyzed the role of miRNA in Non - syndromic cleft lip with or without cleft palate.
    The cKO mice showed lower lip cleft. Real-time PCR analysis and in situ hybridization showed that Gli1 mRNA levels decreased significantly in midline in lower lip of cKO mice. We suggested that the lower lip cleft on the Dicer cKO mice associated with Shh pathway.

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  • Challenges to development of "bioregenerative therapy"

    Grant number：17H06278

    2017 - 2019

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Pioneering)

    Research category：Grant-in-Aid for Challenging Research (Pioneering)

    Awarding organization：Japan Society for the Promotion of Science

    Ohazama Atsushi

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    Grant type：Competitive

    In recent years, stem cells have been discovered in many adult tissues. The presence of stem cells has also been reported in many adult craniofacial region. The aim of this study is to induce tooth using these adult stem cells. We identified the molecular mechanism of controlling stem cells presented in the paratal rugae. Furthermore, we succeeded in inducing signals of tooth formation using stem cells of the palatal rugae.

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  • The Mechanism of Palatal Shelve Induction

    Grant number：17K11829

    2017 - 2019

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    Kawasaki Maiko

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    Grant type：Competitive

    The role of the primary cilia in maxillary bone development is not fully understood. We generated mice with a mesenchymal conditional deletion of Ift88 and Ofd1 using the Wnt1Cre mice. These proteins involved in the function and formation of primary cilia. It has been shown that Ift88 and Ofd1 KO mice exhibit cleft palate and ectopic bone. We also found ectopic apoptosis in the both mutants maxillary process at an early stage of development. To investigate whether the ectopic apoptosis is related to the both maxillary phenotypes, we generated Ift88 and p53 WKO mutants to reduce apoptosis. These mice showed no excess bone formation, suggesting that the cells evading apoptosis by the presence of Ift88 in wild-type mice limit bone formation in maxillary development. On the other hand, the palatal cleft was retained in this mice, indicating that the excess bone formation or abnormal apoptosis was independent of the cleft palate phenotype in Ift88 mutant mice.

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  • Elucidation of control mechanism on stem cell differentiation for tooth regeneration

    Grant number：16H05532

    2016 - 2018

    System name：基盤研究(B)

    Research category：Grant-in-Aid for Scientific Research (B)

    Awarding organization：日本学術振興会

    前田 健康, 医歯学系

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    Grant type：Competitive

    Analysis using Ikkβ-K5 mice with overexpression of NF-kB showed a rapture of ameloblasts, ectopic calcification in dental pulp and morphological changes in cervical loop, a niche of stem cells. Furthermore, we found multiple formation of cervical loop, which is due to an increase in cells of stem cell line as confirmed by an elevation of Sox2. Thereafter, ectopic hair growth and enamel formation as well as supernumerary teeth simultaneously ocurred. These findings indicated that an overexpression of NF-kB induces an increase in stem cell niche and a differentiation of individual stem cell into different tissues. In addition, an elevation of NF-kB around stem cell niche suggests that the differentiation and proliferation of stem cells are controlled by these surrounding stem cells.

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  • The role of primary cilia in amelogenesis

    Grant number：16K20641

    2016 - 2017

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)

    Research category：Grant-in-Aid for Young Scientists (B)

    Awarding organization：Japan Society for the Promotion of Science

    kawasaki katsushige

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    Authorship：Principal investigator  Grant type：Competitive

    Key features of the oral-facial-digital syndrome type 1 (OFD1) include amelogenesis imperfecta (AI). We generated epithelium-specific mutations of Ofd1 using the Cre/loxP -recombination system, and analyzed the role of in amelogenesis.
    The cKO teeth by SEM analysis showed dental attrition of the molar cusps in three-days-old mice as compared to the control. Real-time PCR analysis showed that Gli1 mRNA levels decreased significantly in ameloblasts of cKO mice.
    These results demonstrate that Ofd1 has important roles in Ameligenesis in murine teeth. We suggested that the amelogenesis imperfecta on the Ofd1 cKO mice associated with Shh pathway.

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  • The primary study of the role of the primary cilia in tongue development

    Grant number：26861779

    2014 - 2015

    System name：若手研究(B)

    Research category：Grant-in-Aid for Young Scientists (B)

    Awarding organization：日本学術振興会

    川崎 勝盛, 医歯学系

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    Authorship：Principal investigator  Grant type：Competitive

    In this study, we investigated the role of the primary cilia in tongue development. Mice with neural crest-derived cell conditional mutation of the primary cilia protein, Ofd1, showed notable tongue abnormalities, and the primary cilia were significantly shortened. However, mice with epithelium-, mesoderm- and endoderm-derived cell conditional mutation of Ofd1 exhibited no significant tongue abnormalities, suggesting that the primary cilia in neural crest-derived cells play a critical role in tongue development.

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  • 食物摂取時における一口量調節因子の成長発育変化

    2009

    System name：研究者助成金

    Awarding organization：財団法人富徳会

    川崎 勝盛, 医歯学系

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    Authorship：Principal investigator  Grant type：Competitive

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Teaching Experience (researchmap)

  • 組織学各論

    2015
    Institution name：新潟大学歯学部

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  • 口腔組織発生学

    2015
    Institution name：新潟大学歯学部

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  • 組織学総論

    2015
    Institution name：新潟大学歯学部

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Teaching Experience

  • 顎口腔解剖学演習IA

    2021
    Institution name：新潟大学

  • 基礎歯学ｺｰｽﾜｰｸ(ベーシック形態解析コースII)

    2021
    Institution name：新潟大学

  • 顎口腔解剖学演習IB

    2021
    Institution name：新潟大学

  • 顎口腔解剖学演習IIB

    2021
    Institution name：新潟大学

  • 顎口腔解剖学演習IIA

    2021
    Institution name：新潟大学

  • 基礎歯学ｺｰｽﾜｰｸ(ベーシック形態解析コースI)

    2021
    Institution name：新潟大学

  • 人体のしくみ

    2020
    -
    2021
    Institution name：新潟大学

  • 人体発生学

    2016
    Institution name：新潟大学

  • 組織学各論

    2016
    Institution name：新潟大学

  • 口腔組織発生学

    2016
    Institution name：新潟大学

  • 組織学総論

    2016
    Institution name：新潟大学

  • 基礎科学演習

    2016
    Institution name：新潟大学

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