Prostaglandin E1 protects bone marrow-derived mesenchymal stem cells against serum deprivation-induced apoptosis

Abstract

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 E1 (PGE1) is known to have anti-inflammatory and anti-apoptotic effects on the myocardium. The aim of the present study was to determine whether PGE1 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 PGE1 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 PGE1 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 PGE1 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.

Prostaglandin E1 reduces apoptosis and improves the homing of mesenchymal stem cells in pulmonary arterial hypertension by regulating hypoxia-inducible factor 1 alpha

“…It was shown that treatment with MSCs and PGE1 in rats significantly reduced apoptosis induced by serum deprivation, decreased the protein levels of Bax and caspase-3, and increased that of Bcl-2; however, the underlying mechanism remained unclear [ 28 ]. Prostaglandin E2 (PGE2) can increase HIF-1α expression in hematopoietic stem/progenitor cells (HSPCs), thereby increasing CXCR4 expression and promoting the homing of HSPCs [ 29 ].…”

Mesenchymal stem cells in cardiac regeneration: a detailed progress report of the last 6 years (2010–2015)

“…BM-MSCs have been shown to degrade functionally and quantitatively with increase in age of patients undergoing successful reperfusion treatment, and hence this aspect of the MSCs needs to be explored further [ 95 ]. Prostaglandin E 1 protects BM-MSCs against serum-deprived induced apoptosis by decreasing Bax and caspase-3 expression levels and increasing Bcl-2 expression [ 96 ]. In one study, bone marrow cells derived from heart failure patients were shown to express higher levels of remodelling enzymes and pathways regulating tissue remodelling, scar formation and maturation.…”

Ulinastatin inhibits apoptosis induced by serum deprivation in mesenchymal stem cells

“…One available strategy to enhance MSC survival is treatment with agents that can enhance the viability of MSCs. For example, a previous study reported that prostaglandin E improved MSC survival under H/SD conditions, which is a commonly used model to mimic the ischemic environment in vitro (18). Another study reported that nicorandil protected MSCs from H/SD-induced apoptosis (19).…”