Overexpression of hsa_circ_0001445 reverses oxLDL‑induced inhibition of HUVEC proliferation via SRSF1.

Atherosclerosis is a primary cause of multiple types of cardiovascular disease, including myocardial infarction. In addition, injury of human umbilical vein endothelial cells (HUVECs) can lead to the development of atherosclerosis. Circular (circ)RNAs participate in atherosclerosis. It has previously been shown that circRNA cSMARCA5 (hsa_circ_0001445) expression is downregulated in atherosclerosis. However, the effects of hsa_circ_0001445 on the proliferation of HUVECs remain unclear. In order to mimic atherosclerosis in vitro, HUVECs were treated with oxidized low‑density lipoprotein (oxLDL). The expression levels of specific genes and proteins were detected in HUVECs by reverse transcription‑quantitative PCR and western blot analysis, respectively. Cell proliferation was assessed by Cell Counting Kit‑8 and 5‑Ethynyl‑2'‑deoxyuridine staining. Cell apoptosis and 5,5',6,6'‑Tetrachloro‑1,1',3,3'‑tetraethyl‑imidacarbocyanine staining were examined by flow cytometry. In addition, the association between hsa_circ_0001445 and serine/arginine‑rich splicing factor 1 (SRSF1) was investigated by RNA pull‑down assay. hsa_circ_0001445 expression was downregulated in oxLDL‑treated HUVECs. Moreover, oxLDL‑induced inhibition of HUVEC proliferation was significantly reversed by overexpression of hsa_circ_0001445. oxLDL notably inhibited tube formation and mitochondrial membrane potential in HUVECs, while these effects were markedly reversed by hsa_circ_0001445 overexpression. Furthermore, overexpression of hsa_circ_0001445 reversed oxLDL‑induced activation of β‑catenin by binding to SRSF1. Collectively, these data demonstrated that overexpression of hsa_circ_0001445 reversed oxLDL‑induced inhibition of HUVEC proliferation via activation of the SRSF1/β‑catenin axis. These findings may provide novel targets for the treatment of atherosclerosis.