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Adipose-derived stem cells (ADSCs) possess good proliferative and differentiative abilities, making then a promising candidate for the treatment of cartilage defects. However, local ischemia often causes apoptosis in ADSCs. Transforming growth factor-β3 (TGF-β3) is often used as a chondrogenic differentiation cytokine whose function in apoptosis is unclear. The aim of the present study was to investigate the role of TGF-β3 in ischemia-induced ADSC apoptosis. In the present study, the phenotypes and multipotent differentiation properties of human ADSCs at passage 3 were analyzed using flow cytometry and cytochemical staining. ADSCs were cultured in a serum- and glucose-free medium under hypoxic conditions with or without exogenous TGF-β3 treatment. The apoptosis rate was measured using a TUNEL array and Annexin V/propidium iodide staining. The expression of apoptosis-associated proteins was measured using western blotting. The results revealed ADSCs cultured in normal condition have multi-lineage differentiation potential and high levels of cluster of differentiation (CD)29, CD44 and CD105 expression. Furthermore, ADSCs weakly express CD14, CD34 and CD45, with strong clone formation and migration abilities. Serum deprivation under hypoxic conditions resulted in mitochondria-mediated apoptosis in ADSCs, which was attenuated by exogenous TGF-β3 treatment via upregulation of poly ADP-ribose polymerase (PARP). The results of the present study indicate that TGF-β3 is able to protect ADSCs from ischemia-induced apoptosis via PARP-associated DNA damage repair.

TGF-β3 reduces apoptosis in ischemia-induced adipose-derived stem cells by enhancing DNA repair