TY - JOUR AU - Philipot, Didier AU - Guérit, David AU - Platano, Daniela AU - Chuchana, Paul AU - Olivotto, Eleonora AU - Espinoza, Francisco AU - Dorandeu, Anne AU - Pers, Yves-Marie AU - Piette, Jacques AU - Borzi, Rosa Maria AU - Jorgensen, Christian AU - Noel, Danièle AU - Brondello, Jean-Marc PY - 2014 DA - 2014/02/27 TI - p16INK4a and its regulator miR-24 link senescence and chondrocyte terminal differentiation-associated matrix remodeling in osteoarthritis JO - Arthritis Research & Therapy SP - R58 VL - 16 IS - 1 AB - Recent evidence suggests that tissue accumulation of senescent p16INK4a-positive cells during the life span would be deleterious for tissue functions and could be the consequence of inherent age-associated disorders. Osteoarthritis (OA) is characterized by the accumulation of chondrocytes expressing p16INK4a and markers of the senescence-associated secretory phenotype (SASP), including the matrix remodeling metalloproteases MMP1/MMP13 and pro-inflammatory cytokines interleukin-8 (IL-8) and IL-6. Here, we evaluated the role of p16INK4a in the OA-induced SASP and its regulation by microRNAs (miRs). SN - 1478-6362 UR - https://doi.org/10.1186/ar4494 DO - 10.1186/ar4494 ID - Philipot2014 ER -