C1q/TNF‐related protein‐9 is elevated in hypertension and associated with the occurrence of hypertension‐related atherogenesis

内皮功能障碍 医学 内科学 内分泌学 血管紧张素II 动脉硬化 内皮 下调和上调 血压 生物 生物化学 基因
作者
Qi Zhou,Wenli Cheng,Zuoguang Wang,Jielin Liu,Jing Han,Shaojun Wen,Jinghua Liu
出处
期刊:Cell Biology International [Wiley]
卷期号:45 (5): 989-1000 被引量:3
标识
DOI:10.1002/cbin.11542
摘要

Abstract C1q‐tumor necrosis factor‐related protein‐9 (CTRP9) is an important adipocytokine that is closely associated with cardiovascular disease. This study aimed to detect CTRP9 expression in hypertensive patients and mice and to analyze its effects on hypertension‐related atherogenesis. First, circulating CTRP9 levels were detected in both nonhypertensive subjects and hypertensive patients. The results showed that plasma CTRP9 levels were increased in hypertension patients compared with control subjects and gradually elevated in the Grade I, Grade II, and Grade III groups. While nondipper state did not affect CTRP9 expression in hypertension patients. Hypertension patients with carotid atherosclerotic plaque (CAP) exhibited higher CTRP9 levels and the high CTRP9 group exhibited significantly higher CAP morbidity, CTRP9 levels were positively correlated with the occurrence of CAP. Then, effects of CTRP9 on angiotensin II (Ang II)‐induced endothelial dysfunction were analyzed in vitro, and the results exhibited that treatment with Ang II significantly increased CTRP9 mRNA expression in endothelial cells (ECs), and downregulation of CTRP9 expression aggravated Ang II‐induced endothelial dysfunction in ECs. Mice were infused with Ang II, and CTRP9 was also increased in Ang II‐infused mice and mainly secreted by ECs. In Ang II‐infused ApoE −/− mice, treatment with recombinant CTRP9 significantly reduced atherosclerotic area and alleviated endothelial dysfunction. In conclusion, our results may found that CTRP9 delayed the progression of hypertension‐related arteriosclerosis by alleviating endothelial dysfunction.
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