MicroRNA‑210 improves perfusion recovery following hindlimb ischemia via suppressing reactive oxygen species
- Jinfeng Zhang
- Guotao Rao
- Junying Qiu
- Ronghua He
- Qiongtao Wang
Affiliations: Department of Cardiology, The Central Hospital of Xiaogan, Wuhan University of Science and Technology, Xiaogan, Hubei 432000, P.R. China
- Published online on: October 16, 2020 https://doi.org/10.3892/etm.2020.9366
Copyright: © Zhang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
In peripheral arterial disease (PAD), angiogenesis is a major process involved in repairing the microvasculature in the ischemic lower limb. MicroRNA‑210 (miR‑210) is a microRNA that is substantially increased in patients with PAD. However, the effects of miR‑210 on angiogenesis following PAD remain elusive. In the present study, mice with hindlimb ischemia (HLI) were generated as an animal model of PAD, and miR‑210 levels were overexpressed in the ischemic limb. The overexpression of miR‑210 using microRNA mimics greatly improved angiogenesis and perfusion recovery; in contrast, the knockdown of miR‑210 impaired perfusion recovery 28 days after HLI. Ischemic muscle tissue was harvested 7 days after experimental PAD in order to perform biochemical tests, and miR‑210 antagonism resulted in increased malondialdehyde levels. In cultured endothelial cells under simulated ischemia, miR‑210 mimic improved endothelial cell viability and enhanced tube formation; and a miR‑210 inhibitor decreased cell survival, reduced tube formation and increased reactive oxygen species (ROS) levels. Furthermore, miR‑210 antagonism increased the protein disulfide‑isomerase levels in cultured endothelial cells. These results demonstrate that ischemia‑induced miR‑210 elevation is adaptive in PAD, and that miR‑210 improves angiogenesis at least partially through decreasing ROS production.