Bone morphogenetic protein-2-induced alpha 2 (I) collagen expression in odontoblastic MDPC-23 cells mediated by Smad proteins.
- Author:
Wen-xi HE
1
;
Zhong-ying NIU
;
Shou-liang ZHAO
;
Jie GAO
;
Ping LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Bone Morphogenetic Protein 2; Bone Morphogenetic Proteins; genetics; Cell Line; Collagen; genetics; Collagen Type I; Mice; Odontoblasts; cytology; metabolism; Smad Proteins; physiology; Transforming Growth Factor beta; genetics
- From: Chinese Journal of Stomatology 2004;39(5):386-389
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo characterize the role of Smads proteins in alpha 2 (I) collagen (COL1A2) gene expression induced by bone morphogenetic protein-2 (BMP-2) in odontoblast cell line MDPC-23.
METHODSEndogenous Smad protein expression was determined by immunocytochemistry. Smads function and their role in COL1A2 gene expression were investigated in cotransfection experiments using promoter-luciferase reporter gene construct.
RESULTSMDPC-23 cells expressed Smad1, Smad5 and Smad6. BMP-2 promoted the activation of COL1A2 promoter reporter construct. Transient overexpression of Smad1 or Smad5 was enhanced, while overexpression of Smad6 inhibited BMP-2-induced COL1A2 promoter activity. BMP-2 inducibility could be blocked by overexpression of Smad1 or Smad5 dominant negative mutant.
CONCLUSIONSSmad signaling is functioning and appears to be involved in BMP-2-induced COL1A2 collagen transcription in MDPC-23. Smad signaling may play an important role in odontoblast differentiation and dentin extracellular matrix formation mediated by BMP-2.
