Paracrine effects of human adipose-derived mesenchymal stem cells in inflammatory stress-induced senescence features of osteoarthritic chondrocytes.

Autor:	Platas J; Department of Pharmacology and IDM, University of Valencia, Burjasot, 46100 Valencia, Spain., Guillén MI; Department of Pharmacology and IDM, University of Valencia, Burjasot, 46100 Valencia, Spain.; Department of Pharmacy, Cardenal Herrera-CEU University, Moncada, 46113 Valencia, Spain., Pérez Del Caz MD; Department of Burn and Plastic Surgery, La Fe Polytechnic University Hospital, 46026 Valencia, Spain., Gomar F; Department of Surgery, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain., Castejón MA; Department of Orthopaedic Surgery and Traumatology, De la Ribera University Hospital, Alzira, 46600 Valencia, Spain., Mirabet V; Valencia Transfusion Center, Generalitat Valenciana, 46014 Valencia, Spain., Alcaraz MJ; Department of Pharmacology and IDM, University of Valencia, Burjasot, 46100 Valencia, Spain.
Jazyk:	angličtina
Zdroj:	Aging [Aging (Albany NY)] 2016 Aug; Vol. 8 (8), pp. 1703-17.
DOI:	10.18632/aging.101007
Abstrakt:	Aging and exposure to stress would determine the chondrocyte phenotype in osteoarthritis (OA). In particular, chronic inflammation may contribute to stress-induced senescence of chondrocytes and cartilage degeneration during OA progression. Recent studies have shown that adipose-derived mesenchymal stem cells exert paracrine effects protecting against degenerative changes in chondrocytes. We have investigated whether the conditioned medium (CM) from adipose-derived mesenchymal stem cells may regulate senescence features induced by inflammatory stress in OA chondrocytes. Our results indicate that CM down-regulated senescence markers induced by interleukin-1β including senescence-associated β-galactosidase activity, accumulation of γH2AX foci and morphological changes with enhanced formation of actin stress fibers. Treatment of chondrocytes with CM also decreased the production of oxidative stress, the activation of mitogen-activated protein kinases, and the expression of caveolin-1 and p21. The effects of CM were related to the reduction in p53 acetylation which would be dependent on the enhancement of Sirtuin 1 expression. Therefore, CM may exert protective effects in degenerative joint conditions by countering the premature senescence of OA chondrocytes induced by inflammatory stress. Competing Interests: CONFLICT OF INTERESTS The authors declare no conflict of interests.
Databáze:	MEDLINE
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