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Papers In Press, published online ahead of print June 24, 2002
CNRS UMR 5086, Lyon 69367
Corresponding Author: f.mallein-gerin{at}ibcp.fr
We investigated the effects of bone morphogenetic protein (BMP)-2, a member of the transforming growth factor-
J. Biol. Chem, 10.1074/jbc.M202086200
Submitted on March 4, 2002
Revised on June 10, 2002
Accepted on June 21, 2002
Functions of TGF-
family type I receptors and Smad proteins in the hypertrophic maturation and osteoblastic differentiation of chondrocytes
(TGF-) superfamily, on the regulation of the chondrocyte phenotype and we identified signaling molecules involved in this regulation. BMP-2 triggers three concomitant responses in mouse primary chondrocytes and chondrocytic MC615 cells. First, BMP-2 stimulates expression or synthesis of type II collagen. Second, BMP-2 induces expression of molecular markers characteristic of pre- and hypertrophic chondrocytes, such as Indian hedgehog, PTH/PTHrP receptor, type X collagen and alkaline phosphatase. Third, BMP-2 induces osteocalcin expression, a specific trait of osteoblasts. Constitutively active forms of TGF- family type I receptors and Smad proteins were overexpressed to address their role in this process. ALK-1, ALK-2, ALK-3 and ALK-6 were able to reproduce the hypertrophic maturation of chondrocytes induced by BMP-2. In addition, ALK-2 mimicked further the osteoblastic differentiation of chondrocytes induced by BMP-2. In the presence of BMP-2, Smad1, Smad5 and Smad8 potentiated the hypertrophic maturation of chondrocytes, but failed to induce osteocalcin expression. Smad6 and Smad7 impaired chondrocytic expression and osteoblastic differentiation induced by BMP-2. Thus, our results indicate that Smad-mediated pathways are essential for the regulation of the different steps of chondrocyte and osteoblast differentiation and suggest that additional Smad-independent pathways might be activated by ALK-2.
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