dc.contributor.author | ADININGRAT, ARYA | |
dc.contributor.author | TANIMURA, AYAKO | |
dc.contributor.author | MIYOSHI, KEIKO | |
dc.contributor.author | HAGITA, HIROKO | |
dc.contributor.author | YANUARYSKA, RYNA DWI | |
dc.contributor.author | ARINAWATI, DIAN YOSI | |
dc.contributor.author | HORIGUCHI, TAIGO | |
dc.contributor.author | NOMA, TAKAFUMI | |
dc.date.accessioned | 2017-07-30T03:21:16Z | |
dc.date.available | 2017-07-30T03:21:16Z | |
dc.date.issued | 2016-03 | |
dc.identifier.citation | Adiningrat A, Tanimura A, Miyoshi K, Hagita H, Yanuaryska RD, Arinawati DY, Horiguchi T, Noma T : Isolation and characterization of dental epithelial cells derived from amelogenesis imperfecta rat. Oral Dis 22(2): 132-139, 2016 | en_US |
dc.identifier.issn | 1601-0825 | |
dc.identifier.uri | http://repository.umy.ac.id/handle/123456789/12196 | |
dc.description.abstract | OBJECTIVE: Disruption of the third zinc finger domain of specificity protein 6 (SP6) presents an enamel-specific defect in a rat model of amelogenesis imperfecta (AMI rats). To understand the molecular basis of amelogenesis imperfecta caused by the Sp6 mutation, we established and characterized AMI-derived rat dental epithelial (ARE) cells.
MATERIALS AND METHODS: ARE cell clones were isolated from the mandibular incisors of AMI rats, and amelogenesis-related gene expression was analyzed by reverse transcription polymerase chain reaction (RT-PCR). Localization of wild-type SP6 (SP6WT) and mutant-type SP6 (SP6AMI) was analyzed by immunocytochemistry. SP6 transcriptional activity was monitored
by rho-associated protein kinase 1 (Rock1) promoter activity with its specific binding to the promoter region in dental (G5 and ARE) and non-dental (COS-7) epithelial cells.
RESULTS: Isolated ARE cells were varied in morphology and gene expression. Both SP6WT and SP6AMI
were mainly detected in nuclei. The promoter analysis revealed that SP6WT and SP6AMI enhanced Rock1 promoter activity in G5 cells but that enhancement by SP6AMI was weaker, whereas no enhancement was observed in the ARE and COS-7 cells, even though SP6WT and SP6AMI bound to the promoter in all instances.
CONCLUSION: ARE cell clones can provide a useful in vitro model to study the mechanism of SP6-mediated amelogenesis imperfecta. | en_US |
dc.description.sponsorship | This work was partly supported by Grants-in-Aid for scientific research (Nos. 23592735 to TN and 21791805 to KM) from the
Ministry of Education, Culture, Sports, Science and Technology of Japan; the Presidential Research Budget of the University of
Tokushima; a fellowship from the Directorate General of Higher Education, Ministry of Education, Republic of Indonesia (No.
934/E4.4/K/2011 to AA); and by a research grant from KAO Health Science Research (TN). We thank the Support Center for
Advanced Medical Science in the Faculty of Dentistry at the University of Tokushima for their technical assistance. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Oral Diseases - John Wiley & Sons Ltd | en_US |
dc.subject | amelogenesis imperfecta | en_US |
dc.subject | Sp6 mutation | en_US |
dc.subject | amelogenesis imperfecta in vivo model | en_US |
dc.subject | isolation and characterization dental epithelial cells | en_US |
dc.title | ISOLATION AND CHARACTERIZATION OF DENTAL EPITHELIAL CELLS DERIVED FROM AMELOGENESIS IMPERFECTA RAT | en_US |
dc.title.alternative | Establishment of an in vitro AI disease model | en_US |
dc.type | Article | en_US |