Runx2 inhibits chondrocyte proliferation and hypertrophy through its expression in the perichondrium
2006; Cold Spring Harbor Laboratory Press; Volume: 20; Issue: 21 Linguagem: Inglês
10.1101/gad.1482906
ISSN1549-5477
AutoresEiichi Hinoi, Peter Bialek, You‐Tzung Chen, Marie-Therese Rached, Yoram Groner, Richard R. Behringer, David M. Ornitz, Gérard Karsenty,
Tópico(s)TGF-β signaling in diseases
ResumoThe perichondrium, a structure made of undifferentiated mesenchymal cells surrounding growth plate cartilage, regulates chondrocyte maturation through poorly understood mechanisms. Analyses of loss- and gain-of-function models show that Twist-1, whose expression in cartilage is restricted to perichondrium, favors chondrocyte maturation in a Runx2-dependent manner. Runx2, in turn, enhances perichondrial expression of Fgf18 , a regulator of chondrocyte maturation. Accordingly, compound heterozygous embryos for Runx2 and Fgf18 deletion display the same chondrocyte maturation phenotype as Fgf18 -null embryos. This study identifies a transcriptional basis for the inhibition of chondrocyte maturation by perichondrium and reveals that Runx2 fulfills antagonistic functions during chondrogenesis.
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