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Research Paper|Volume 12, Issue 14|pp 14365—14375

Circular RNA circVEGFC accelerates high glucose-induced vascular endothelial cells apoptosis through miR-338-3p/HIF-1α/VEGFA axis

Hua Wei1, Cong Cao1, Xiaojuan Wei2, Minglv Meng3, Biaoliang Wu1, Lianxin Meng1, Xi Wei1, Shixing Gu1, Hongmian Li4
  • 1Department of Endocrinology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533022, Guangxi, China
  • 2Urology Care Unit, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533022, Guangxi, China
  • 3Medical Statistics Office, Youjiang Medical University for Nationalites, Baise 533022, Guangxi, China
  • 4Department of Plastic and Aesthetic Surgery, The Fifth Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi, China
* Co-first authors
Received: February 15, 2020Accepted: May 27, 2020Published: July 17, 2020
https://doi.org/10.18632/aging.103478

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.

Abstract

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.