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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 3542149, 13 pages
Research Article

Inhibition of Caveolae Contributes to Propofol Preconditioning-Suppressed Microvesicles Release and Cell Injury by Hypoxia-Reoxygenation

1Department of Anesthesiology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China
2Department of Anesthesiology, Taihe Hospital, Hubei University of Medicine, Anesthesiology Research Institute of Hubei University of Medicine, Shiyan, Hubei Province, China
3Department of Anesthesiology, Dongfeng General Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, China
4Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Affiliated Cancer Hospital & Institute, Guangzhou Medical University, Guangzhou 511436, China
5Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute of Neurology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China

Correspondence should be addressed to Du Feng and Liangqing Zhang

Received 7 June 2017; Accepted 6 August 2017; Published 19 September 2017

Academic Editor: Hong Zheng

Copyright © 2017 Fan Deng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Endothelial microvesicles (EMVs), released after endothelial cell (EC) apoptosis or activation, may carry many adverse signals and propagate injury by intercellular transmission. Caveolae are 50–100 nm cell surface plasma membrane invaginations involved in many pathophysiological processes. Recent evidence has indicated EMVs and caveolae may have functional effects in cells undergoing H/R injury. Propofol, a widely used anaesthetic, confers antioxidative stress capability in the same process. But the connection between EMVs, H/R, and caveolae remains largely unclear. Here, we found that H/R significantly increased the release of EMVs, the expression of CAV-1 (the structural protein responsible for maintaining the shape of caveolae), oxidative stress, and the mitochondrial damage, and all these changes were inhibited by propofol preconditioning. Interestingly, the caveolae inhibitor Mβ-CD strengthened the protective effect of propofol preconditioning. We further found that the release of EMVs is more significantly reduced under propofol preconditioning in the presence of the caveolae inhibitor Mβ-CD. EMVs released from H/R-treated cells caused a substantially increased mitochondrial and cellular damage to normal HUVECs after 4 hours of coculture. Thus, we conclude that inhibition of caveolae contributes to propofol preconditioning-suppressed microvesicles release and cell injury by H/R.