| miR-328-5p functions as a critical negative regulator in early endothelial inflammation and advanced atherosclerosis |
Yangxia Zhang1,# (Co-Author), Yingke Li1,# (Co-Author), Zhisheng Han1 (Co-Author), Qingyang Huo1 (Co-Author), Longkai Ji1 (Co-Author), Xuejia Liu3 (Co-Author), Han Li3 (Corresponding Author), Xinxing Zhu  1,4,* (Corresponding Author), Zhipeng Hao2 (Corresponding Author) |
1Henan Joint International Research Laboratory of Stem Cell Medicine, Xinxiang Medical University,
2Department of thoracic surgery of Tongji Hospital, Huazhong University of Science & Technology,
3College of Life Science and Technology, Xinxiang Medical University,
4Anhui Province Key Laboratory of Clinical and Preclinical Research in Respiratory Disease, First Affiliated Hospital, Bengbu Medical University, |
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Abstract
Early proatherogenic inflammation constitutes a significant risk factor for atherogenesis development. Despite this, the precise molecular mechanisms driving this pathological progression remain largely 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 towards 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.
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| Abstract, Accepted Manuscript [Submitted on April 10, 2024, Accepted on June 10, 2024] |
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