miR-328-5p functions as a critical negative regulator in early endothelial inflammation and advanced atherosclerosis

Early proatherogenic inflammation constitutes a significant risk factor for atherogenesis development. Despite this, the precise molecular mechanisms driving this pathological progression largely remain elusive. Our study unveils a pivotal role for the microRNA miR-328-5p in dampening endothelial in...

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Published in:BMB reports 2024, 57(8), , pp.375-380
Main Authors: Yangxia Zhang, Yingke Li, Zhisheng Han, Qingyang Huo, Longkai Ji, Xuejia Liu, Han Li, Xinxing Zhu, Zhipeng Hao
Format: Article
Language:English
Subjects:
화학
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Summary:Early proatherogenic inflammation constitutes a significant risk factor for atherogenesis development. Despite this, the precise molecular mechanisms driving this pathological progression largely remain elusive. Our study unveils a pivotal role for the microRNA miR-328-5p in dampening endothelial inflammation by modulating the stability of JUNB (JunB proto-oncogene). Perturbation of miR-328-5p levels results in heightened monocyte adhesion to endothelial cells and enhanced transendothelial migration, while its overexpression mitigates these inflammatory processes. Furthermore, miR-328-5p hinders macrophage polarization toward the pro-inflammatory M1 phenotype, and exerts a negative influence on atherosclerotic plaque formation in vivo. By pinpointing JUNB as a direct miR-328-5p target, our research underscores the potential of miR-328-5p as a therapeutic target for inflammatory atherosclerosis. Reintroduction of JUNB effectively counteracts the anti-atherosclerotic effects of miR-328-5p, highlighting the promise of pharmacological miR-328-5p targeting in managing inflammatory atherosclerosis. KCI Citation Count: 0
ISSN:1976-6696
1976-670X
DOI:10.5483/BMBRep.2024-0055