Inhibition of miR-155 attenuates abdominal aortic aneurysm in mice by regulating macrophage-mediated inflammation
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Updated: Feb 14, 2026

Porcine Model of Infrarenal Abdominal Aortic Aneurysm
Published on: November 21, 2019
Zhidong Zhang1,2, Kai Liang1,2, Gangqiang Zou1,2
1Department of Vascular and Endovascular Surgery, Henan Provincial People's Hospital, NO.7 Weiwu Road, Zhengzhou, Henan 450003. P.R. China.
Abstract:
The aim of the present study was to identify abdominal aortic aneurysms (AAA)-associated miR-155 contributing to AAA pathology by regulating macrophage-mediated inflammation. Angiotensin II (AngII)-infused apolipoprotein E-deficient (ApoE-/-) mice and THP-1 cells model of miR-155 overexpression and deficiency were used in the experiments. The expression of miR-155 was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Cytokines were evaluated using enzyme-linked immunoabsorbent assay (ELISA). Western blotting was used to measure the levels of MMP-2, MMP-9, iNOS, and monocyte chemoattractant protein (MCP)-1 proteins. Immunostaining and transwell were used to determine CD68, elastic collagen, proliferation, and migration of vascular smooth muscle cells (VSMCs). The results showed that miR-155 and cytokines were up-regulated in AAA patients or ApoE-/- mice. Overexpression of miR-155 enhanced MMP-2, MMP-9, iNOS, and MCP-1 levels, and stimulated the proliferation and migration of VSMCs. Meanwhile, inhibition of miR-155 had the opposite effect. In addition, histology demonstrated accumulation of CD68 and elastic collagen-positive areas significantly decreased in miR-155 antagomir injection group. In conclusion, the results of the present study suggest that inhibiting miR-155 is crucial to prevent the development of AAA by regulating macrophage inflammation.
Insights
This study reveals microRNA-155 (miR-155) promotes abdominal aortic aneurysm (AAA) by increasing inflammation. Inhibiting miR-155 significantly reduced AAA development in mouse models, highlighting its therapeutic potential.
Area of Science:
- Vascular Biology
- Molecular Medicine
- Inflammation Research
Background:
- Abdominal aortic aneurysms (AAA) are characterized by inflammation and extracellular matrix degradation.
- MicroRNAs (miRNAs) play critical roles in cardiovascular diseases, but their specific role in AAA pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the role of miR-155 in AAA development.
- To determine if miR-155 regulates macrophage-mediated inflammation in AAA pathology.
Main Methods:
- Utilized Angiotensin II-infused apolipoprotein E-deficient (ApoE-/-) mice and THP-1 cell models.
- Assessed miR-155 expression via qRT-PCR.
- Quantified protein levels (MMP-2, MMP-9, iNOS, MCP-1) using Western blotting and ELISA.
- Evaluated cellular changes (CD68, elastic collagen, VSMC proliferation/migration) through immunostaining and transwell assays.
Main Results:
- miR-155 and associated inflammatory cytokines were upregulated in AAA patients and mouse models.
- miR-155 overexpression exacerbated AAA pathology by increasing MMPs, iNOS, MCP-1, and VSMC activity.
- Inhibition of miR-155 using antagomirs reduced inflammatory markers and pathological features in mice.
Conclusions:
- miR-155 is a key mediator in AAA development, primarily by promoting macrophage-driven inflammation.
- Inhibiting miR-155 presents a promising therapeutic strategy for preventing AAA progression.
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