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

    Author(s)
    Wang, Jiawan
    Schilling, Jan M
    Niesman, Ingrid R
    Headrick, John P
    Finley, J Cameron
    Kwan, Evan
    Patel, Piyush M
    Head, Brian P
    Roth, David M
    Yue, Yun
    Patel, Hemal H
    Griffith University Author(s)
    Headrick, John P.
    Year published
    2014
    Metadata
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    Abstract
    Background:: Caveolae 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. Methods:: Mice were exposed to isoflurane or oxygen vehicle (30 min, ᳶ h pertussis toxin pretreatment, an irreversible Gi inhibitor). Caveolin trafficking, cardioprotective "survival kinase" signaling, mitochondrial function, and ultrastructure were assessed. Results:: Isoflurane increased ...
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    Background:: Caveolae 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. Methods:: Mice were exposed to isoflurane or oxygen vehicle (30 min, ᳶ h pertussis toxin pretreatment, an irreversible Gi inhibitor). Caveolin trafficking, cardioprotective "survival kinase" signaling, mitochondrial function, and ultrastructure were assessed. Results:: Isoflurane increased cardiac caveolae (n = 8 per group; data presented as mean ᠓D for Ctrl versus isoflurane; [caveolin-1: 1.78 ᠰ.12 vs. 3.53 ᠰ.77; P < 0.05]; [caveolin-3: 1.68 ᠰ.29 vs. 2.67 ᠰ.46; P < 0.05]) and mitochondrial caveolin levels (n = 16 per group; [caveolin-1: 0.87 ᠰ.18 vs. 1.89 ᠮ19; P < 0.05]; [caveolin-3: 1.10 ᠰ.29 vs. 2.26 ᠰ.28; P < 0.05]), and caveolin-enriched mitochondria exhibited improved respiratory function (n = 4 per group; [state 3/complex I: 10.67 ᠱ.54 vs. 37.6 ᠷ.34; P < 0.05]; [state 3/complex II: 37.19 ᠴ.61 vs. 71.48 ᠱ5.28; P < 0.05]). Isoflurane increased phosphorylation of survival kinases (n = 8 per group; [protein kinase B: 0.63 ᠰ.20 vs. 1.47 ᠰ.18; P < 0.05]; [glycogen synthase kinase 3ߺ 1.23 ᠰ.20 vs. 2.35 ᠰ.20; P < 0.05]). The beneficial effects were blocked by pertussis toxin. Conclusions:: Gi 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. In mice, cardiac preconditioning from isoflurane involved increased caveolin levels in mitochondria and their associated improved respiratory function. These effects were blocked by pretreatment with Gi inhibitors, suggesting that agents that target Gi and caveolin trafficking may serve as cardioprotective agents.
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    Journal Title
    Anesthesiology
    Volume
    121
    Issue
    3
    DOI
    https://doi.org/10.1097/ALN.0000000000000295
    Subject
    Cardiology (incl. cardiovascular diseases)
    Clinical sciences
    Publication URI
    http://hdl.handle.net/10072/69927
    Collection
    • Journal articles

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