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Updated: Dec 5, 2025

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
miRNA 146b-5p protects against atherosclerosis by inhibiting vascular smooth muscle cell proliferation and migration
Dating Sun1, Gui Xiang2, Jing Wang1
1Department of Internal Medicine, Division of Cardiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, PR China.
Abstract:
Aim: To explore the potentially important role of miRNA 146b-5p (miR-146b) during the development of atherosclerosis. Materials & methods: Proliferation, migration and luciferase assays and mouse models were used to determine the functions of miR-146b. Results: miR-146b was identified as substantially upregulated in the aortic plaques of ApoE-/- mice as well as in response to inflammatory cytokines. Overexpression of miR-146b repressed proliferation and migration of vascular smooth muscle cells by downregulating Bag1 and Mmp16, respectively. Adeno-associated virus-mediated miR-146b overexpression inhibited neointima formation after carotid injury and suppressed atherosclerotic plaque formation in Western diet-induced ApoE-/- mice. Conclusion: miR-146b is a novel regulator of vascular smooth muscle cell function induced by inflammatory response, specifically in neointima formation, and offers a novel therapeutic strategy for treating atherosclerosis.
Insights
MicroRNA 146b-5p (miR-146b) plays a key role in atherosclerosis development. Upregulation of miR-146b in vascular cells inhibits plaque formation, suggesting it as a therapeutic target.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- MicroRNA Therapeutics
Background:
- Atherosclerosis is a chronic inflammatory disease.
- MicroRNAs (miRNAs) are implicated in cardiovascular disease pathogenesis.
- The specific role of miR-146b in atherosclerosis requires further elucidation.
Purpose of the Study:
- To investigate the function of miR-146b in the development of atherosclerosis.
- To determine the regulatory mechanisms of miR-146b in vascular smooth muscle cells.
- To assess the therapeutic potential of miR-146b in atherosclerosis models.
Main Methods:
- In vitro assays: proliferation, migration, and luciferase assays.
- In vivo studies: mouse models including ApoE-/- mice and carotid injury models.
- Molecular analysis: assessment of gene expression (Bag1, Mmp16) and miRNA levels.
Main Results:
- miR-146b was significantly upregulated in atherosclerotic plaques and inflammatory conditions.
- Overexpression of miR-146b suppressed vascular smooth muscle cell proliferation and migration by downregulating Bag1 and Mmp16.
- Adeno-associated virus-mediated miR-146b delivery inhibited neointima formation and atherosclerotic plaque progression in mice.
Conclusions:
- miR-146b is a novel regulator of vascular smooth muscle cell function in response to inflammation.
- miR-146b plays a protective role in neointima formation and atherosclerosis.
- miR-146b represents a potential therapeutic target for atherosclerosis treatment.
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