Abstract
► We found miR-483-5p downregulated in HUVECs under hypoxia. ► We found that overexpression of miR-483-5p inhibited angiogenesis in vitro. ► We found inhibition of miR-483-5p promoted angiogenesis in vitro. ► We found miR-483-5p targeted serum response factor directly.
Angiogenesis, a key factor in ischemic heart disease, is rapidly initiated in response to hypoxic or ischemic conditions. MicroRNAs (miRNAs) are endogenously expressed small non-coding RNAs that regulate gene expression at post-transcriptional level. The recent discovery of the involvement of these RNAs in the control of angiogenesis renders them very attractive in the development of new approaches for restoring the angiogenic balance. In the present study, we explored that miR-483-5p, a microRNA embedded in the intron of insulin-like growth factor 2 (Igf2), acts as an endogenous angiogenesis-inhibiting factor. We identified that serum response factor (SRF) is one of miR-483-5p target genes. These findings indicated that the miR-483-5p-SRF pathway may offer a novel strategy for treatment with angiogenesis in ischemic heart disease patients.