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Circular RNA circVEGFC accelerates high glucose-induced vascular endothelial cells apoptosis through miR-338-3p/HIF-1α/VEGFA axis
- Source :
- Aging (Albany NY)
- Publication Year :
- 2020
- Publisher :
- Impact Journals, LLC, 2020.
-
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.
- Subjects :
- Vascular Endothelial Growth Factor A
Aging
vascular endothelial cells
Vascular Endothelial Growth Factor C
Apoptosis
circVEGFC
Umbilical vein
Hypoxia-Inducible Factor 1-Alpha
Transcription (biology)
Circular RNA
Human Umbilical Vein Endothelial Cells
Humans
Transcription factor
Gene knockdown
Chemistry
Endothelial Cells
circular RNA
RNA, Circular
Cell Biology
Hypoxia-Inducible Factor 1, alpha Subunit
VEGF
high glucose
Up-Regulation
Cell biology
MicroRNAs
Vascular endothelial growth factor A
Glucose
Gene Expression Regulation
Research Paper
Subjects
Details
- ISSN :
- 19454589
- Volume :
- 12
- Database :
- OpenAIRE
- Journal :
- Aging
- Accession number :
- edsair.doi.dedup.....a6653230b9402d79b08b21bc5777c292