AI Article Synopsis
- - Hypoxia influences the process of reparative angiogenesis, which is crucial for healing and is regulated by various factors, including microRNAs (miRNAs).
- - The study identifies miR-130a as a key player in how hypoxia affects human endothelial colony-forming cells (ECFCs), enhancing their ability to promote blood vessel formation under low oxygen conditions.
- - MiR-130a increases the levels of VEGFR2, activates the STAT3 pathway, and boosts HIF1α through translational inhibition, revealing its role in improving the regenerative capacity of endothelial cells during hypoxia.
Article Abstract
Hypoxia modulates reparative angiogenesis, which is a tightly regulated pathophysiological process. MicroRNAs (miRNAs) are important regulators of gene expression in hypoxia and angiogenesis. However, we do not yet have a clear understanding of how hypoxia-induced miRNAs fine-tune vasoreparative processes. Here, we identify miR-130a as a mediator of the hypoxic response in human primary endothelial colony-forming cells (ECFCs), a well-characterized subtype of endothelial progenitors. Under hypoxic conditions of 1% O, miR-130a gain-of-function enhances ECFC pro-angiogenic capacity and potentiates their vasoreparative properties . Mechanistically, miR-130a orchestrates upregulation of VEGFR2, activation of STAT3, and accumulation of HIF1α via translational inhibition of . These findings unveil a new role for miR-130a in hypoxia, whereby it activates the VEGFR2/STAT3/HIF1α axis to enhance the vasoregenerative capacity of ECFCs.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7869000 | PMC |
| http://dx.doi.org/10.1016/j.omtn.2021.01.015 | DOI Listing |
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