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Tenascin-c renders a proangiogenic phenotype in macrophage via annexin II.

Journal of cellular and molecular medicine (2017-09-01)
Zhiyang Wang, Qi Wei, Liang Han, Keqing Cao, Tianfeng Lan, Zhenjie Xu, Yingjuan Wang, Yuan Gao, Jing Xue, Fei Shan, Jun Feng, Xin Xie
ABSTRACT

Tenascin-c is an extracellular matrix glycoprotein, the expression of which relates to the progression of atherosclerosis, myocardial infarction and heart failure. Annexin II acts as a cell surface receptor of tenascin-c. This study aimed to delineate the role of tenascin-c and annexin II in macrophages presented in atherosclerotic plaque. Animal models with atherosclerotic lesions were established using ApoE-KO mice fed with high-cholesterol diet. The expression of tenascin-c and annexin II in atherosclerotic lesions was determined by qRT-PCR, Western blot and immunohistochemistry analysis. Raw 264.7 macrophages and human primary macrophages were exposed to 5, 10 and 15 μg/ml tenascin-c for 12 hrs. Cell migration as well as the proangiogenic ability of macrophages was examined. Additionally, annexin II expression was delineated in raw 264.7 macrophages under normal condition (20% O

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Sigma-Aldrich
MISSION® esiRNA, targeting human ANXA2

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