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Heat stress causes dysfunctional autophagy in oxidative skeletal muscle

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dc.contributor.authorBrownstein, Alexandra J.en
dc.contributor.authorGanesan, Shanthien
dc.contributor.authorSummers, Corey M.en
dc.contributor.authorPearce, Sarah C.en
dc.contributor.authorHale, Benjamin J.en
dc.contributor.authorRoss, Jason W.en
dc.contributor.authorGabler, Nicholas K.en
dc.contributor.authorSeibert, Jacob T.en
dc.contributor.authorRhoads, Robert P.en
dc.contributor.authorBaumgard, Lance H.en
dc.contributor.authorSelsby, Joshua T.en
dc.contributor.departmentAnimal and Poultry Sciencesen
dc.date.accessioned2019-08-28T16:26:07Zen
dc.date.available2019-08-28T16:26:07Zen
dc.date.issued2017-06en
dc.description.abstractWe have previously established that 24h of environmental hyperthermia causes oxidative stress and have implicated mitochondria as likely contributors to this process. Given this, we hypothesized that heat stress would lead to increased autophagy/mitophagy and a reduction in mitochondrial content. To address this hypothesis pigs were housed in thermoneutral (TN; 20 degrees C) or heat stress (35 degrees C) conditions for 1- (HS1) or 3- (HS3) days and the red and white portions of the semitendinosus collected. We did not detect differences in glycolytic muscle. Counter to our hypothesis, upstream activation of autophagy was largely similar between groups as were markers of autophagosome nucleation and elongation. LC3A/B-I increased 1.6-fold in HS1 and HS3 compared to TN (P < 0.05), LC3A/B-II was increased 4.1-fold in HS1 and 4.8-fold in HS3 relative to TN, (P < 0.05) and the LC3A/B-II/I ratio was increased 3-fold in HS1 and HS3 compared to TN suggesting an accumulation of autophagosomes. p62 was dramatically increased in HS1 and HS3 compared to TN. Heat stress decreased mitophagy markers PINK1 7.0-fold in HS1 (P < 0.05) and numerically by 2.4-fold in HS3 compared to TN and BNIP3L/NIX by 2.5-fold (P < 0.05) in HS1 and HS3. Markers of mitochondrial content were largely increased without activation of PGC-1 signaling. In total, these data suggest heat-stress-mediated suppression of activation of autophagy and autophagosomal degradation, which may enable the persistence of damaged mitochondria in muscle cells and promote a dysfunctional intracellular environment.en
dc.description.notesThis project was supported by USDA grants 2014-67015-21627 (JTS) and 20116700330007 (LHB) and AB was supported by the Wise Burrough's fund.en
dc.description.sponsorshipUSDA [2014-67015-21627, 20116700330007]; Wise Burrough's funden
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.14814/phy2.13317en
dc.identifier.issn2051-817Xen
dc.identifier.issue12en
dc.identifier.othere13317en
dc.identifier.pmid28646096en
dc.identifier.urihttp://hdl.handle.net/10919/93280en
dc.identifier.volume5en
dc.language.isoenen
dc.publisherThe Physiological Societyen
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectHeat strokeen
dc.subjecthyperthermiaen
dc.subjectmitochondriaen
dc.subjectmitophagyen
dc.subjectoxidative stressen
dc.titleHeat stress causes dysfunctional autophagy in oxidative skeletal muscleen
dc.title.serialPhysiological Reportsen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten

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