NFI-C가 Smad와 TGF-βR1의 발현에 미치는 영향

Abstract

NFI-C null mice demonstrated aberrant odontoblast differentiation, abnormal dentin formation, and thus molar lacking roots while other tissues/organs in the body, including ameloblasts appear to be unaffected and normal. Abnormal denin in NFI-C null mice shared morphological similarities to osteodentin that is formed as a result of dental caries. However, little is known about the interrelationship between NFI-C and osteodentin formation. In this study, in order to elucidate the molecular characteristics of abnormal odntoblast in NFI-C null mice, we examined the expression of Ask-1, Cdc-2, Smad2/3, and TGF-βR1 in the cell culture and tissue sections of NFI-C null mice using immunofluorescence and immunohistochemistry. The results were as follows: 1. NFI-C protein was localized in the nucleus and cytoplasm of the normal odontoblasts in vitro. 2. Ask-1 and Cdc-2 protein was expressed in the perinuclear cytoplasm of both normal and NFI-C null mice. There were any differences in the expression pattern of Ask-1 and CDc-2 protein between normal and NFI-C null mice. 3. Smad2/3 was not expressed in the odontoblast and subodontoblastic cells of the normal mice, whereas NFI-C null mice expressed the Smad2/3 immunoreactivity in the odontoblast and subodontoblastic cells of the tooh pulp. 4. TGF-βR1 was also nearly expressed in the odontoblast and subodontoblastic cells of the normal mice, whereas TGF-βR1 immunoreactivity was strongly detected in the subodontoblastic cells of the NFI-C null mice. These results suggest that disruption of NFI-C increased the expression of Smad2/3 and TGF-βR1 in developing odontoblasts and consequently caused the abnormal dentin formation which is similar to osteodentin.