BACKGROUND

In our previous study, through integrative transcriptomic and ChIP-seq analysis, we revealed that ETV1 is a potential transcription factor involved in ventricular remodeling in the early stage of MI. This study aims to investigate the regulatory roles of ETV1 and whether ETV1 regulates angiogenesis after MI.

METHODS

In this study, MI model was induced by ligating the left anterior descending coronary artery. The expression of was modulated via intramyocardial injection of adeno-associated virus serotype 9 (AAV9) with endothelial-specific promoter . Fibrosis was determined by Masson staining and apoptosis was assessed by TUNEL staining. Angiogenesis was evaluated by CD31 immunofluorescence staining. For experiments, HUVECs were transfected with overexpression lentivirus, and wound healing and tube formation assays were performed to validate the angiogenic role of . Western blot was conducted to determine the level of angiogenetic factors and the underlying mechanisms.

RESULTS

The expression of was decreased in the hearts of MI mice, as well as in isolated cardiac microvascular endothelial cells (CMECs). Moreover, overexpression of alleviated the deterioration of heart function, mitigated the fibrosis, reduced apoptosis, and promoted angiogenesis after MI. Moreover, overexpression enhanced migration and tube formation abilities of HUVECs. Mechanistically, ETV1 upregulated the expression of VEGFA, VEGFR2, and eNOS.

CONCLUSIONS

In summary, Etv1 promote angiogenesis via activating VEGFA/VEGFR2/eNOS pathway after MI, which further ameliorate adverse ventricular remodeling. These results suggest that ETV1 may serve as a potential target for the treatment of myocardial infarction.