Functional analysis of endoplasmic reticulum stress in the progression of cartilage degeneration

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We investigated the role of proapoptotic transcription factor Chop in murine chondrocyte apoptosis and in the progression of cartilage degeneration, using Chop-knockout (Chop-/-) chondrocytes and model of surgically-induced osteoarthritis (OA) in Chop-/- mice. Our results indicate that Chop plays a direct role in chondrocyte apoptosis and that endoplasmic reticulum (ER) stress-mediated apoptosis contributes to the progression of cartilage degeneration in mice. We also investigated the role of ER stress sensor Perk, Ire1alpha, and Atf6alpha in cartilage degeneration and chondrocyte metabolism with Perk+/-, Ire1alpha+/-, and Atf6alpha-/- mouse models of OA and these genes-knockdown chondrocytes. The results suggest that Atf6alpha involves the progress of cartilage degeneration and the expression of Ire1alpha and Atf6alpha relates with chondrocyte anabolism.