The lncRNA ANRIL regulates endothelial dysfunction by targeting the let-7b/TGF-βR1 signalling pathway
Autor: | Qingyuan Yang, Xianglan Liu, Tuo Huang, Yong Sun, Song Sun, Jing Li, Guosheng Fu, Ying Liu, Nan Gu, Jian Wu, Shufeng Li, Hui Dong, Yang Yi, Bo Yu |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Physiology Clinical Biochemistry Receptor Transforming Growth Factor-beta Type I Smad Proteins SMAD Models Biological Umbilical vein Proinflammatory cytokine 03 medical and health sciences 0302 clinical medicine medicine Human Umbilical Vein Endothelial Cells Humans RNA Messenger Endothelial dysfunction Acute Coronary Syndrome Inflammation Gene knockdown Base Sequence business.industry Cell Biology medicine.disease Hedgehog signaling pathway Long non-coding RNA Up-Regulation MicroRNAs 030104 developmental biology 030220 oncology & carcinogenesis Cancer research RNA Long Noncoding business Biomarkers Transforming growth factor Signal Transduction |
Zdroj: | Journal of cellular physiologyREFERENCES. 236(3) |
ISSN: | 1097-4652 |
Popis: | The long noncoding RNA antisense noncoding RNA in the INK4 locus (ANRIL) plays a critical role in the development of atherosclerosis. However, the precise effect of ANRIL on endothelial dysfunction remains unclear. In this study, we investigated ANRIL expression in patients with coronary artery disease and elucidated the molecular mechanism underlying its effect. ANRIL expression was detected in the blood plasma of 111 patients. We analysed the correlation between ANRIL and endothelial dysfunction markers. We also examined the effect of ANRIL on the regulation of endothelial dysfunction. ANRIL levels were increased in patients with acute coronary syndrome. The expression of ANRIL is associated with the inflammatory cytokines monocyte chemoattractant protein-1 and interleukin-10, which are secreted in response to endothelial dysfunction. Knockdown of ANRIL significantly promoted cell proliferation and tubule formation and inhibited inflammatory activation and apoptosis of human umbilical vein endothelial cells (HUVEC). ANRIL-mediated inhibition of let-7b regulates HUVEC dysfunction by targeting the TGF-βR1/Smad signalling pathway. This study highlights a new therapeutic strategy for preventing endothelial dysfunction associated with cardiovascular disease. |
Databáze: | OpenAIRE |
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