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Updated: Dec 2, 2025
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
MicroRNA-210 improves perfusion recovery following hindlimb ischemia via suppressing reactive oxygen species
Jinfeng Zhang1,2, Guotao Rao1, Junying Qiu1
1Department of Cardiology, The Central Hospital of Xiaogan, Wuhan University of Science and Technology, Xiaogan, Hubei 432000, P.R. China.
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.
Insights
MicroRNA-210 (miR-210) promotes blood vessel repair in peripheral arterial disease (PAD). Overexpressing miR-210 improved limb perfusion in a mouse model, while inhibiting it worsened recovery and increased oxidative stress.
Area of Science:
- Vascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Peripheral arterial disease (PAD) involves impaired microvasculature repair in the lower limb.
- Angiogenesis is crucial for restoring blood flow in ischemic tissues.
- MicroRNA-210 (miR-210) levels are elevated in PAD patients, but its role in angiogenesis is unclear.
Purpose of the Study:
- To investigate the functional role of miR-210 in angiogenesis and perfusion recovery in a mouse model of peripheral arterial disease.
- To determine the effects of miR-210 modulation on endothelial cell function under ischemic conditions.
Main Methods:
- Hindlimb ischemia (HLI) model in mice to simulate PAD.
- Overexpression and knockdown of miR-210 using microRNA mimics and inhibitors.
- Assessment of angiogenesis, limb perfusion recovery, and biochemical markers (malondialdehyde, reactive oxygen species).
- In vitro studies using cultured endothelial cells under simulated ischemia.
Main Results:
- Overexpression of miR-210 significantly enhanced angiogenesis and perfusion recovery in HLI mice.
- Knockdown of miR-210 impaired perfusion recovery and increased malondialdehyde levels.
- In vitro, miR-210 mimic improved endothelial cell viability and tube formation, while inhibiting it reduced cell survival, tube formation, and increased reactive oxygen species (ROS).
- miR-210 antagonism increased protein disulfide-isomerase levels in endothelial cells.
Conclusions:
- Ischemia-induced elevation of miR-210 is an adaptive response in peripheral arterial disease.
- miR-210 promotes angiogenesis and perfusion recovery, at least partly by reducing oxidative stress (ROS production).
- Targeting miR-210 may offer a therapeutic strategy for improving outcomes in PAD patients.
