In:
Oral Diseases, Wiley, Vol. 22, No. 2 ( 2016-03), p. 132-139
Abstract:
Disruption of the third zinc finger domain of specificity protein 6 ( SP 6) 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 SP 6 ( SP 6 WT ) and mutant‐type SP 6 ( SP 6 AMI ) was analyzed by immunocytochemistry. SP 6 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 SP 6 WT and SP 6 AMI were mainly detected in nuclei. The promoter analysis revealed that SP 6 WT and SP 6 AMI enhanced Rock1 promoter activity in G5 cells but that enhancement by SP 6 AMI was weaker, whereas no enhancement was observed in the ARE and COS ‐7 cells, even though SP 6 WT and SP 6 AMI bound to the promoter in all instances. Conclusion ARE cell clones can provide a useful in vitro model to study the mechanism of SP 6‐mediated amelogenesis imperfecta.
Type of Medium:
Online Resource
ISSN:
1354-523X
,
1601-0825
DOI:
10.1111/odi.2016.22.issue-2
Language:
English
Publisher:
Wiley
Publication Date:
2016
detail.hit.zdb_id:
2008428-6
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