• Anesthesiology · Sep 2014

    Cardioprotective Trafficking of Caveolin to Mitochondria Is Gi-protein Dependent.

    • Jiawan Wang, Jan M Schilling, Ingrid R Niesman, John P Headrick, J Cameron Finley, Evan Kwan, Piyush M Patel, Brian P Head, David M Roth, Yun Yue, and Hemal H Patel.
    • From the Department of Anesthesiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China (J.W., Y.Y.); VA San Diego Healthcare System, San Diego, California (P.M.P., B.P.H., D.M.R., H.H.P.); Department of Anesthesiology, University of California, San Diego, California (J.M.S., I.R.N., J.C.F., E.K., P.M.P., B.P.H., D.M.R., H.H.P.); and Heart Foundation Research Center, Griffith University, Gold Coast, Queensland, Australia (J.P.H.).
    • Anesthesiology. 2014 Sep 1; 121 (3): 538-48.

    BackgroundCaveolae are a nexus for protective signaling. Trafficking of caveolin to mitochondria is essential for adaptation to cellular stress though the trafficking mechanisms remain unknown. The authors hypothesized that G protein-coupled receptor/inhibitory G protein (Gi) activation leads to caveolin trafficking to mitochondria.MethodsMice were exposed to isoflurane or oxygen vehicle (30 min, ± 36 h pertussis toxin pretreatment, an irreversible Gi inhibitor). Caveolin trafficking, cardioprotective "survival kinase" signaling, mitochondrial function, and ultrastructure were assessed.ResultsIsoflurane increased cardiac caveolae (n = 8 per group; data presented as mean ± SD for Ctrl versus isoflurane; [caveolin-1: 1.78 ± 0.12 vs. 3.53 ± 0.77; P < 0.05]; [caveolin-3: 1.68 ± 0.29 vs. 2.67 ± 0.46; P < 0.05]) and mitochondrial caveolin levels (n = 16 per group; [caveolin-1: 0.87 ± 0.18 vs. 1.89 ± .19; P < 0.05]; [caveolin-3: 1.10 ± 0.29 vs. 2.26 ± 0.28; P < 0.05]), and caveolin-enriched mitochondria exhibited improved respiratory function (n = 4 per group; [state 3/complex I: 10.67 ± 1.54 vs. 37.6 ± 7.34; P < 0.05]; [state 3/complex II: 37.19 ± 4.61 vs. 71.48 ± 15.28; P < 0.05]). Isoflurane increased phosphorylation of survival kinases (n = 8 per group; [protein kinase B: 0.63 ± 0.20 vs. 1.47 ± 0.18; P < 0.05]; [glycogen synthase kinase 3β: 1.23 ± 0.20 vs. 2.35 ± 0.20; P < 0.05]). The beneficial effects were blocked by pertussis toxin.ConclusionsGi proteins are involved in trafficking caveolin to mitochondria to enhance stress resistance. Agents that target Gi activation and caveolin trafficking may be viable cardioprotective agents.

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