Literature DB >> 28038796

Cyclophilin A mediates the ox-LDL-induced activation and apoptosis of macrophages via autophagy.

Zhiqiang Xue1, Wei Yuan2, Jing Li1, Hong Zhou1, Lihua Xu1, Jiayi Weng1, Xiaoyang Li1, Xinru Zhang1, Zhongqun Wang1, Jinchuan Yan3.   

Abstract

BACKGROUND: Oxidized low-density lipoprotein (ox-LDL) is the most common inflammatory factor that mediates the activation and apoptosis of macrophages. Cyclophilin A (CyPA) is expressed following oxidative stress, hypoxia, and infection. However, the role of CyPA in the activation and apoptosis of macrophages is unclear. The aims of the study were to determine whether CyPA mediates the ox-LDL-induced activation and apoptosis in RAW264.7 cells and to analyze potential mechanisms. METHODS AND
RESULTS: Through Western blot and ELISA test, the expression of CyPA induced by ox-LDL is time-dependent in RAW264.7 cells. Gene silencing of CyPA reduced the generation of lipid droplets in the cytoplasm and downregulated the expression of the surface markers of macrophage activation, namely, CD80, CD86, and major histocompatibility complex class 2 antigen. Cell apoptosis is significantly decreased and the level of anti-apoptosis protein bcl-2 is increased in CyPA silent cells compared with the control group. Finally, autophagy-related protein LC3-II/LC3-I ratio level significantly decreased in CyPA silent cells with less autophagosome formation while the blocked autophagy flux was recovered. The differences in the activation and apoptosis between CyPA silent cells and the control cells were inhibited by pre-treatment with class III PI 3-kinase inhibitor 3-MA.
CONCLUSIONS: These results indicate that CyPA mediates the ox-LDL-induced activation and apoptosis in RAW264.7 cells by regulating autophagy.
Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Entities:  

Keywords:  Apoptosis; Atherosclerosis; Autophagy; CyclophilinA; Macrophages; Oxidized low-density lipoprotein

Mesh:

Substances:

Year:  2016        PMID: 28038796     DOI: 10.1016/j.ijcard.2016.12.042

Source DB:  PubMed          Journal:  Int J Cardiol        ISSN: 0167-5273            Impact factor:   4.164


  6 in total

1.  NR4A1 contributes to high-fat associated endothelial dysfunction by promoting CaMKII-Parkin-mitophagy pathways.

Authors:  Pei Li; Yuzhi Bai; Xia Zhao; Tian Tian; Liying Tang; Jing Ru; Yun An; Jing Wang
Journal:  Cell Stress Chaperones       Date:  2018-02-22       Impact factor: 3.667

2.  Cyclophilin A Protects Cardiomyocytes against Hypoxia/Reoxygenation-Induced Apoptosis via the AKT/Nox2 Pathway.

Authors:  Fuyu Cheng; Wei Yuan; Mengfei Cao; Rui Chen; Xiuli Wu; Jinchuan Yan
Journal:  Oxid Med Cell Longev       Date:  2019-04-28       Impact factor: 6.543

3.  Polysaccharide from Fuzi protects against Ox‑LDL‑induced calcification of human vascular smooth muscle cells by increasing autophagic activity.

Authors:  Lizhen Liao; Xiaodong Zhuang; Weidong Li; Qibiao Su; Jie Zhao; Ying Liu
Journal:  Mol Med Rep       Date:  2018-01-25       Impact factor: 2.952

4.  Insulin‑receptor substrate 1 protects against injury in endothelial cell models of ox‑LDL‑induced atherosclerosis by inhibiting ER stress/oxidative stress‑mediated apoptosis and activating the Akt/FoxO1 signaling pathway.

Authors:  Juan Liu; Xu Yi; Yuan Tao; Yanjiang Wang; Zhiqiang Xu
Journal:  Int J Mol Med       Date:  2020-09-15       Impact factor: 4.101

5.  Ivabradine Induces Cardiac Protection against Myocardial Infarction by Preventing Cyclophilin-A Secretion in Pigs under Coronary Ischemia/Reperfusion.

Authors:  Ignacio Hernandez; Laura Tesoro; Rafael Ramirez-Carracedo; Javier Diez-Mata; Sandra Sanchez; Marta Saura; Jose Luis Zamorano; Carlos Zaragoza; Laura Botana
Journal:  Int J Mol Sci       Date:  2021-03-12       Impact factor: 5.923

Review 6.  The Role of Cyclophilins in Inflammatory Bowel Disease and Colorectal Cancer.

Authors:  Lifang Liang; Rongxiao Lin; Ying Xie; Huaqing Lin; Fangyuan Shao; Wen Rui; Hongyuan Chen
Journal:  Int J Biol Sci       Date:  2021-06-16       Impact factor: 6.580

  6 in total

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