Objective: To investigate the role of follistatin-like protein 1 (FSTL1) on bone marrow mesenchymal stem cells (BM-MSCs)-mediated cardioprotection during myocardial ischemia/reperfusion injury.
Methods: Rat bone marrow mesenchymal stem cells were isolated by whole bone marrow adherence method in vitro. A total of 60 Wistar rats were randomly divided into 4 groups: control group, ischemic /reperfusion injury (IRI) group, ischemia/reperfusion injury group treated with natural BM-MSCs (IRI+ MSC group), ischemia/reperfusion injury group treated with BM-MSCs which did not contain FSTL1 (IRI+ MSC FSTL1 siRNA group). Survival analysis was used to analyze survival time of rats, besides, expression of FSTL1 was detected by Western blotting. Myocardial pathological changes were detected by Hematoxylin and Eosin (HE) staining. Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) and enzyme-linked immunosorbent assay (ELISA) were used to determine the associated biomarkers and apoptosis 7 days after operation.
Results: Compared with IRI group, rats in IRI+ MSC group had a higher survival rate and lived longer. Meanwhile, IRI+ MSC group had higher FSTL1 expression in blood and myocardial tissues than IRI group. Control group showed significantly lower apoptosis rate of myocardial cells[(1.4±0.1)% vs (29.8±4.5)%, P<0.05], less histological changes and infarction areas (0 vs 24.48±4.27, P<0.05) than IRI group. Compared with IRI group, IRI+ MSC group had an improvement of apoptosis rate[(4.2±0.3)% vs (29.8±4.5)%, P<0.05], less histological injury and infarction areas (15.12±3.82 vs 24.48±4.27, P<0.01). IRI+ MSC group had lower expression of LDH, MDA, CK and higher expression of SOD than IRI group (P<0.05). However, IRI+ MSC FSTL1 siRNA group showed weaker protection of myocardial cells than IRI+ MSC group after knockdown of FSTL1 (P<0.05).
Conclusion: FSTL1, which was secreted by BM-MSCs, plays a protective role in myocardial IRI.