Objective
Cartilage hypocellularity due to cell death contributes to the development of OA. Experimental exposure to MIA results in either chondrocyte necrosis (in vitro) or experimental OA with apoptosis when injected ia (in vivo). As Hsp-70 is known to protect from cell death, we have evaluated the beneficial properties of its over-expression or induction in rat chondrocyte cells (RCC) after MIA exposure.