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

Abstract

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.

• Authors: Fan Deng, Shuang Wang, Shuyun Cai, Zhe Hu, Riping Xu, Jingjing Wang, Du Feng, Liangqing Zhang
• Journal: Oxidative medicine and cellular longevity (Oxid Med Cell Longev) Vol. 2017 Pg. 3542149 ( 2017) ISSN: 1942-0994 [Electronic] United States
• PMID: 29181124 (Publication Type: Journal Article)

Chemical References

• Propofol

Topics

• Apoptosis
• Caveolae (metabolism)
• Cell Hypoxia
• Humans
• Propofol (metabolism)