分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

Vaspin attenuates the progression of atherosclerosis by inhibiting ER stress‑induced macrophage apoptosis in apoE‑/‑ mice

Ying Lin, Jianhui Zhuang, Hailing Li, Guofu Zhu, Shunping Zhou, Weiming Li, Wenhui Peng, Yawei Xu

Journal:Molecular Medicine Reports

IF:1.55

DOI:10.3892/mmr.2015.4708

PMID:26708512

Published:2015-12-22

research field:生物材料心脏病学纳米技术治疗学

Abstract

Visceral adipose tissue‑derived serine protease inhibitor (vaspin) is a novel adipokine with potential insulin‑sensitizing properties, which was initially detected in the visceral adipose tissue of genetically obese rats. Previous studies have demonstrated that vaspin exerts a protective effect on arteries undergoing atherosclerosis in vitro, and it has been shown to exert anti‑inflammatory and antimigratory effects on vascular smooth muscle cells. Vaspin promotes proliferation and inhibits apoptosis in endothelial cells, and decreases proliferation of the arterial intima under diabetic conditions. In addition, macrophage apoptosis is an important characteristic of atherosclerotic plaque development. In vivo experiments were performed by histological analysis, including Oil Red O, hematoxylin and eosin and Masson's trichrome staining. Mice were injected with lentivirus via the tail vein and tissues were obtained for histological analysis. Cell apoptosis was determined by flow cytometry of Annexin‑V/propidium iodide dual staining and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling assay. Total proteins were extracted and protein expression levels were detected by western blot analysis. The present study aimed to investigate whether vaspin was able to protect against atherosclerotic development in vivo, and to explore the underlying mechanisms of the potential antiatherogenic effects. The results of the current study indicated that vaspin inhibited the progression of atherosclerotic plaques in apoE‑/‑ mice by inhibiting endoplasmic reticulum stress‑induced macrophage apoptosis.

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