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

• Published in: BMB reports Vol. 57; no. 8; pp. 375 - 380
• Main Authors: Zhang, Yangxia, Li, Yingke, Han, Zhisheng, Huo, Qingyang, Ji, Longkai, Liu, Xuejia, Li, Han, Zhu, Xinxing, Hao, Zhipeng
• Format: Journal Article
• Language: English
• Published: Korea (South) 생화학분자생물학회 01.08.2024
• Subjects: Animals; Atherosclerosis - genetics; Atherosclerosis - metabolism; Atherosclerosis - pathology; Cell Adhesion - genetics; Cell Movement - genetics; Endothelial Cells - metabolism; Endothelial Cells - pathology; Human Umbilical Vein Endothelial Cells - metabolism; Humans; Inflammation - genetics; Inflammation - metabolism; Inflammation - pathology; Macrophages - metabolism; Mice; MicroRNAs - genetics; MicroRNAs - metabolism; Monocytes - metabolism; Plaque, Atherosclerotic - genetics; Plaque, Atherosclerotic - metabolism; Plaque, Atherosclerotic - pathology; Proto-Oncogene Mas; 화학
• ISSN: 1976-6696; 1976-670X
• DOI: 10.5483/BMBRep.2024-0055

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. [BMB Reports 2024; 57(8): 375-380].