Prostaglandin E(1) protects bone marrow-derived mesenchymal stem cells against serum deprivation-induced apoptosis

Mesenchymal stem cells (MSCs) have become a recent focus of experimental and clinical research regarding myocardial regeneration. However, the therapeutic potential of these cells is limited by poor survival. Prostaglandin E(1) (PGE(1)) is known to have anti-inflammatory and anti-apoptotic effects on the myocardium. The aim of the present study was to determine whether PGE(1) could protect MSCs against serum deprivation (SD)-induced apoptosis. An SD model was used to induce apoptosis in MSCs in vitro. Apoptotic morphological changes were detected by Hoechst 33258 fluorescent nuclear staining; and Annexin V-fluorescein isothiocyanate/propidium iodide (PI) double staining and flow cytometry was used to quantify the rate of apoptosis. Western blot analysis was used to detect the expression levels of the apoptosis-associated proteins Bcl-2, Bax and caspase-3. The results of the present study demonstrated that SD induced apoptosis of MSCs, and that treatment with PGE(1) attenuated the morphological changes characteristic of apoptosis. Annexin V/PI staining showed that the rate of apoptosis gradually increased with the duration of ischemia. Furthermore, treatment with PGE(1) significantly reduced SD-induced apoptosis, decreased the protein expression levels of Bax and caspase-3, and increased the expression levels of Bcl-2. These data suggest that PGE(1) is able to influence the survival of MSCs under certain conditions. These results may aid in improving the therapeutic efficacy of MSC transplantation used to treat chronic ischemic heart disease.