Research Paper Advance Articles
Circular RNA circVEGFC accelerates high glucose-induced vascular endothelial cells apoptosis through miR-338-3p/HIF-1α/VEGFA axis
- 1 Department of Endocrinology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533022, Guangxi, China
- 2 Urology Care Unit, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533022, Guangxi, China
- 3 Medical Statistics Office, Youjiang Medical University for Nationalites, Baise 533022, Guangxi, China
- 4 Department of Plastic and Aesthetic Surgery, The Fifth Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi, China
Received: February 15, 2020 Accepted: May 27, 2020 Published: July 17, 2020https://doi.org/10.18632/aging.103478
How to Cite
Copyright © 2020 Wei et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
More and more findings illustrate the critical roles of circular RNA (circRNA) in diabetes mellitus (DM) and its complications. A major pathological characteristic for DM is the apoptosis of endothelial cells (ECs) induced by high glucose (HG), however, the function of circRNA in the ECs’ phenotypes is still elusive. Here, this study identified an up-regulated circRNA (circVEGFC) in the HG-induced human umbilical vein endothelial cells (HUVECs). Functionally, knockdown of circVEGFC alleviated the apoptosis and recovered the proliferation in HUVECs induced by HG administration. Mechanistically, circVEGFC functioned as the sponge of miR-338-3p, and miR-338-3p was found to target the 3’-Untranslated Regions (3’-UTR) of hypoxia inducible factor 1 alpha (HIF-1α). HIF-1α, a critical transcription factor in DM, could activate the transcription of vascular endothelial growth factor A (VEGFA) and promote its protein product. In conclusion, these findings reveal the promotion of circVEGFC/miR-338-3p/HIF-1α/VEGFA axis in the HG-induced ECs’ apoptosis, providing a potential treatment strategy for ECs’ damage in DM.