Key result
SDF-1-BMSCs significantly improved cardiac function, increased Bcl-2 and VEGF, and lowered TNF-α compared to BMSCs alone or control in rats with ischemia/reperfusion injury (P<0.05).
Why the study?
Acute myocardial infarction carries high mortality, and whether SDF-1 can repair ischemia/reperfusion-induced heart injury by regulating BMSC proliferation remained to be investigated.
Answers are grounded in this paper and cite their sources.
SDF-1 enhances the therapeutic efficacy of BMSCs in repairing ischemia/reperfusion myocardial injury by promoting cell proliferation and inhibiting apoptosis in a preclinical model.
Acute myocardial infarction (AMI) is a serious disease with a high mortality. Stromal cell-derived factor 1 (SDF-1) can recruit circulating progenitor cell populations into damaged tissues. Bone marrow mesenchymal stem cells (BMSCs) have a variety of cellular functions. We studied the ability of SDF-1 to repair ischemia/reperfusion injury (IRI)-induced heart injury via regulating BMSCs proliferation in rats. Mouse BMSCs were isolated and expanded. Cell proliferation and apoptotic factors were analyzed. The rats were assigned into control group, BMSCs group or SDF-1-BMSCs group. SDF-1 expression was analyzed by ELISA. Rat heart function changes, the expression of various related factors, and the secretion of TNF-α were analyzed. SDF-1 stimulated BMSCs proliferation and decreased Caspase 3 activity (P <0.05). Rats in BMSCs group and SDF-1-BMSCs group showed significantly improved cardiac function, higher expressions of Bcl-2 and VEGF, and lower levels of TNF-α (P < 0.05), while the improvement in SDF-1-BMSCs group was the most significant (P <0.05). In conclusion, SDF-1 promotes the repair of IRI via promoting the proliferation of BMSCs and inhibiting apoptosis.
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Zhang et al. (2022) studied Ischemia/reperfusion injury (IRI)-induced heart injury. SDF-1-BMSCs vs. Control group and BMSCs group was evaluated on Cardiac function, expressions of Bcl-2 and VEGF, and levels of TNF-α (p=<0.05). SDF-1-BMSCs significantly improved cardiac function, increased Bcl-2 and VEGF, and lowered TNF-α compared to BMSCs alone or control in rats with ischemia/reperfusion injury (P<0.05).
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