[Bone morphogenetic protein-2-induced alpha 2 (I) collagen expression in odontoblastic MDPC-23 cells mediated by Smad proteins].
OBJECTIVE
To 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.


METHODS
Endogenous 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.


RESULTS
MDPC-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.


CONCLUSIONS
Smad 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.
He
Wen-xi
WX
Department of Operative Dentistry, College of Stomatology, The Fourth Military Medical University, Xi'an 710032, China. hwenxi@yahoo.com.cn
Niu
Zhong-ying
ZY
Zhao
Shou-liang
SL
Gao
Jie
J
Li
Ping
P
D000818:Animals; D055396:Bone Morphogenetic Protein 2; D019485:Bone Morphogenetic Proteins / Q000235:genetics*; D002460:Cell Line; D003094:Collagen / Q000235:genetics*; D024042:Collagen Type I; D051379:Mice; D009804:Odontoblasts / Q000166:cytology / Q000378:metabolism*; D051785:Smad Proteins / Q000502:physiology*; D016212:Transforming Growth Factor beta / Q000235:genetics*
C525719:Bmp2 protein, mouse; D055396:Bone Morphogenetic Protein 2; D019485:Bone Morphogenetic Proteins; D024042:Collagen Type I; D051785:Smad Proteins; D016212:Transforming Growth Factor beta; D003094:Collagen