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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,
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.
Abstract, Accepted Manuscript [Submitted on April 10, 2024, Accepted on June 10, 2024]
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