The Protective Role of the Pericellular Matrix in Chondrocyte Apoptosis

Abstract

The PCM, a native microenvironment of chondrocytes, protects chondrocytes from apoptosis. Type VI collagen is a functional component of the PCM that contributes to the survival of chondrocytes.

Computational investigation of in situ chondrocyte deformation and actin cytoskeleton remodelling under physiological loading

“…Furthermore, it has been demonstrated that collagen VI, the dominant collagen type in the PCM, functions in protecting the chondrocyte from apoptosis [83]. The present study shows that the PCM plays a role in stress transfer to the cell, with significant implications for cytoskeletal remodelling.…”

Matrix-Embedded Cytokines to Simulate Osteoarthritis-Like Cartilage Microenvironments

“…33 In early stages of OA the balance between degradation and synthesis of the pericellular matrix of chondrocytes is disturbed. 37 Animal models of secondary (posttraumatic) OA showed enhanced synthesis of collagen 2 and aggrecan, 38 as well as abnormal ECM components. Transgenic mice expressing mutant aggrecan, lacking a key aggrecanase cleavage site, demonstrated that erosion of ECM is the key event in the biomechanical failure of the OA joint, irrespective of whether the initiating cause was driven by inflammation (antigen-induced arthritis) or biomechanics (meniscectomy-induced).…”

Annexin A2 mediates collagen VI secretion, pulmonary elasticity, and bronchial epithelial cell apoptosis

“…Interestingly, soluble COL6 appears to prevent apoptosis of serum-starved fibroblasts by suppressing the pro-apoptotic protein, Bax (Rühl et al, 1999). In avian corneal fibroblasts, cell viability depends specifically on the interaction between matrix-associated COL6 and cellmembrane-associated b1 integrins (Howell and Doane, 1998), and COL6 also appears to protect chondrocytes, neurons and cardiac myocytes from apoptosis due to chemical inducers, ultraviolet irradiation or early, but not late, tissue infarction, respectively (Cheng et al, 2011;Luther et al, 2012;Peters et al, 2011). In Col6a1 2/2 mice, myofibers undergo apoptotic cell death in a process thought to reflect opening of the cyclosporine-A-sensitive, mitochondrial permeability transition pore, which might be triggered by integrin-mediated induction of reactive oxygen species or defective regulation of autophagy (Grumati et al, 2010;Irwin et al, 2003).…”