ArticleExperimental and therapeutic medicine2020
MicroRNA-210 improves perfusion recovery following hindlimb ischemia via suppressing reactive oxygen species.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- ROS-scavenging ultrasonicated graphene oxide/alginate microgels for mesenchymal stem cell delivery and hindlimb ischemia treatment.Materials today. Bio · 2024Article
- Skeletal muscle MiR-210 expression is associated with mitochondrial function in peripheral artery disease patients.Translational research : the journal of laboratory and clinical medicine · 2022Article
- Molecular Mechanisms Associated with ROS-Dependent Angiogenesis in Lower Extremity Artery Disease.Antioxidants (Basel, Switzerland) · 2021Review
- MicroRNAs in peripheral artery disease: potential biomarkers and pathophysiological mechanisms.Therapeutic advances in cardiovascular diseaseArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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