NFI-C 결손 생쥐의 치수세포에서 cDNA microarray를 이용한

Abstract

NFI-C null mice demonstrated aberrant odontoblast differentiation, abnormal dentin formation, and thus molar lacking roots. However, other tissues/organs in the body including ameloblasts appeared to be unaffected and normal. However, little is known about the mechanism of NFI-C function in odontoblast differentiation and tooth root formation. In this study, in order to elucidate the molecular mechanism of abnormal root formation in NFI-C null mice, we compared the gene expression patterns in the primary pulp cells of normal and NFI-C null mice using cDNA microarray.

1. According to the cDNA microarray profile comparison, the expression of TGFβ and TGFβ-RI showed up-regulation in NFI-C null primary pulp cells. Interestingly, the cDNA microarray showed that most of the Smad genes were down-regulated in the NFI-C null primary pulp cells compared with normal cells. Western blot analysis demonstrated a dramatic increased level of the expression of TGFβ-RI and p-Smad2/3 proteins in the NFI-C null primary pulp cells compared to that of normal. The expression of TGF-β1 was also up-regulated in the NFI-C null primary pulp cells. 2. Also, the cDNA microarray showed that most of the FGFs gene expression were down-regulated in the NFI-C null primary pulp cells compared with normal cells. 3. cDNA microarray analysis exhibited that p16 and p18 were up-regulated in NFI-C null primary pulp cells, but cyclin E1 and cyclin D1 were down-regulated in the NFI-C null primary pulp cells. The NFI-C null primary pulp cells showed an increase in p21 as well as p16 expression, and a decrease in cyclin D1 as well as cyclin B1 expression compared with normal cells by western blot analysis.

These results indicate that disturbance of the Nfic gene suppresses odontogenic cell proliferation of aberrant odontoblasts by up-regulating the expression of TGFβ-RI and its downstream signaling molecules during root formation, contributing to the formation of short roots.