Inhibition of beta-catenin signaling in articular chondrocytes results in articular cartilage destruction.

ABSTRACT:

Objective

Osteoarthritis is a degenerative joint disease whose molecular mechanism is currently unknown. Wnt/beta-catenin signaling has been demonstrated to play a critical role in the development and function of articular chondrocytes. To determine the role of beta-catenin signaling in articular chondrocyte function, we generated Col2a1-ICAT-transgenic mice to inhibit beta-catenin signaling in chondrocytes.

Methods

The expression of the ICAT transgene was determined by immunostaining and Western blot analysis. Histologic analyses were performed to determine changes in articular cartilage structure and morphology. Cell apoptosis was determined by TUNEL staining and the immunostaining of cleaved caspase 3 and poly(ADP-ribose) polymerase (PARP) proteins. Expression of Bcl-2, B

SUBMITTER: Zhu M 

PROVIDER: S-EPMC2667964 | biostudies-literature | 2008 Jul

REPOSITORIES: biostudies-literature