Vascular smooth muscle cells (VSMCs) has been reported to be implicated in atherosclerotic plaque instability and rupture. Recently, it has been demonstrated that VSMCs block the progression of cardiac remodeling and thus promoting cardiac function in a rat myocardial infarction model. However, the detailed molecular mechanism of how VSMCs contributes to recovery in myocardial ischemia/reperfusion remains not fully understood.

We have isolated, identified and cultured VSMCs from rats to co-culture with rat cardiomyocyte H9C2. To culture H9C2 cells under hypoxia, we utilized CoCl₂-containing medium to culture for 8 h and then was replaced with normal media for additional 16 h. Cell viability was examined by MTT assay and apoptosis was determined by flow cytometry. Infarcted area of myocardial tissue was measured by TTC staining.

VSMCs was shown to promote cell viability and inhibit apoptosis of H9C2 cells under hypoxia, which exhibited upregulated anti-apoptotic protein Bcl-2 and autophagy-related protein p62, whereas pro-apoptotic protein cleaved caspase-3 and the level of LC3II/LC3I were downregulated. Then, we confirmed VSMCs played the contributory role in cell viability of H9C2 under hypoxia by secreting bFGF, which exerted its function through PI3K/Akt pathway. Finally, in vivo, the results demonstrated that VSMCs transplantation contributed to recovery of myocardial ischemia.

We determine that VSMCs promote recovery of infarcted cardiomyocyte through secretion of bFGF, which then activating PI3K/Akt pathway to inhibit apoptosis and autophagy. These findings provide more insights into the molecular mechanism underlying VSMCs contributing to recovery of myocardial I/R and facilitate developing therapeutical strategies for treating heart diseases.