Overexpression and induction of heat shock protein 70 protect chondrocytes from cell death in vitro and in vivo

Abstract

Osteoarthritis (OA) is characterized by fibrillation and erosion of hyaline cartilage, subchondral bone sclerosis and osteophyte formation at the joint margins. These changes, resulting from poorly understood events, lead to both cartilage matrix degradation and inhibition of matrix component synthesis. Moreover, cartilage hypocellularity due to cell death (apoptosis or necrosis) contributes to the development of OA. Heat shock protein 70 (Hsp70) plays a protective role as a molecular chaperone in cells by facilitating the folding, intracellular transport, assembly, and disassembly of proteins. An increase in the expression of Hsp70 in chondrocytes has been associated with the severity of OA lesions and could be an indicator of the early stages of OA. Some experiments recently demonstrated that Hsp70 protects cells from death induced by stresses, mechanical and biological factors.