Original ArticlePropofol Provides Cardiac Protection by Suppressing the Proteasome Degradation of Caveolin-3 in Ischemic/Reperfused Rat HeartsZhu, Afang MD*,†; Wei, Xin MD†; Zhang, Yali MD†; You, Tao MD‡; Yao, Shanglong MD, PhD†; Yuan, Shiying MD, PhD†; Xu, Haodong MD, PhD§; Li, Faqian MD, PhD¶; Mao, Weike MD†Author Information *Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China; †Department of Anesthesiology, Peking Union Medical College Hospital, CAMS&PUMC, Beijing, People's Republic of China; ‡Department of Cardiology, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China; §Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA; and ¶Department of Laboratory Medicine and Pathology, University of Minnesota, MN. Reprints: Weike Mao, MD, Department of Anesthesiology and Intensive Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China (e-mail: [email protected]). Supported by grants from the National Natural Science Foundation of China (NO: 81270239). The authors report no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.jcvp.org). A. Zhu and X. Wei have contributed equally to this work. Journal of Cardiovascular Pharmacology: March 2017 - Volume 69 - Issue 3 - p 170-177 doi: 10.1097/FJC.0000000000000454 Buy SDC Erratum Metrics Abstract The mechanisms underlying propofol's cardioprotective role remain elusive. Caveolin-3 (Cav-3) has been shown to mediate both opioids- and volatile anesthetics-induced cardioprotection against ischemia/reperfusion (I/R) injury. We hypothesize that the cardioprotective role of propofol is mediated through Cav-3 and its regulation of PI3K/Akt/GSK3β signal pathway. Rats or H9c2 cardiomyocytes were exposed to propofol before I/R or simulated ischemia/reperfusion (SI/R). Propofol pretreatment significantly decreased left ventricle infarct size in vivo (P < 0.05) and terminal deoxynucleotidyl transferase nick-end labeling-positive cells both in vivo and in vitro (P < 0.05), along with an increased Cav-3 protein expression and binding of Cav-3 to p85-subunit of PI3K. No significant change in Cav-3 mRNA expression in left ventricle tissues was found in either I/R or propofol-treated groups. Methyl-β-cyclodextrin or Cav-3 siRNA was used to knockdown Cav-3 expression in vitro, which virtually abolished propofol-induced cardiac protection and PI3K/Akt/GSK3β pathway activation. In contrast, MG132, a proteasome inhibitor, could significantly restore SI/R-induced Cav-3 decrease. It is concluded that Cav-3 mediates propofol-induced cardioprotection against I/R injury and the relevant PI3K/Akt/GSK3β activation. The downregulation of Cav-3 under SI/R may be caused by proteasome degradation, and this process can be prevented by propofol. Erratum In the article that appeared on pages 170-177 of the March 2017 issue, the affiliation for authors Xin Wei, Yali Zhang, Shanglong Yao, Shiying Yuan, and Weike Mao was incorrectly listed as the Department of Anesthesiology, Peking Union Medical College Hospital, CAMS&PUMC, Beijing, People’s Republic of China. The correct affiliation is the Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China. Journal of Cardiovascular Pharmacology. 70(2):128, August 2017. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.