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Acute heat stress activated inflammatory signaling in porcine oxidative skeletal muscle

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dc.contributor.authorGanesan, Shanthien
dc.contributor.authorVolodina, Olgaen
dc.contributor.authorPearce, Sarah C.en
dc.contributor.authorGabler, Nicholas K.en
dc.contributor.authorBaumgard, Lance H.en
dc.contributor.authorRhoads, Robert P.en
dc.contributor.authorSelsby, Joshua T.en
dc.contributor.departmentAnimal and Poultry Sciencesen
dc.date.accessioned2018-01-10T15:30:06Zen
dc.date.available2018-01-10T15:30:06Zen
dc.date.issued2017-08en
dc.description.abstractDespite well-studied clinical manifestations, intracellular mechanisms of prolonged hyperthermic injury remain unclear, especially in skeletal muscle. Given muscle's large potential to impact systemic inflammation and metabolism, the response of muscle cells to heat-mediated injury warrants further investigation. We have previously reported increased activation of NF-κB signaling and increased NF-κB and AP-1-driven transcripts in oxidative skeletal muscle following 12 h of heat stress. The purpose of this investigation was to examine early heat stress-induced inflammatory signaling in skeletal muscle. We hypothesized that heat stress would increase NF-κB and AP-1 signaling in oxidative skeletal muscle. To address this hypothesis, 32 gilts were randomly assigned to one of four treatment groups (n = 8/group): control (0 h: 21°C) or exposed to heat stress conditions (37°C) for 2 h (n = 8), 4 h (n = 8), or 6 h (n = 8). Immediately following environmental exposure pigs were euthanized and the red portion of the semitendinosus muscle (STR) was harvested. We found evidence of NF-κB pathway activation as indicated by increased protein abundance of NF-κB activator IKK-α following 4 h and increased total NF-κB protein abundance following 6 h of heat stress. Heat stress also stimulated AP-1 signaling as AP-1 protein abundance was increased in nuclear fractions following 4 h of heat stress. Interleukin-6 protein abundance and activation of the JAK/STAT pathway were decreased in heat stressed muscle. These data indicate that heat stress activated inflammatory signaling in the porcine STR muscle via the AP-1 pathway and early activation of the NF-κB pathway.en
dc.description.versionPublished versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.14814/phy2.13397en
dc.identifier.eissn2051-817Xen
dc.identifier.issue16en
dc.identifier.orcidRhoads, RP [0000-0002-5205-5834]en
dc.identifier.urihttp://hdl.handle.net/10919/81670en
dc.identifier.volume5en
dc.language.isoenen
dc.relation.urihttps://www.ncbi.nlm.nih.gov/pubmed/28830980en
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectAP‐1en
dc.subjectJak Staten
dc.subjectNF‐κBen
dc.subjectheat strokeen
dc.subjecthyperthermiaen
dc.subjectinflammationen
dc.titleAcute heat stress activated inflammatory signaling in porcine oxidative skeletal muscleen
dc.title.serialPhysiological Reportsen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dcterms.dateAccepted2017-07-27en
pubs.organisational-group/Virginia Techen
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciencesen
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciences/Animal and Poultry Sciencesen
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciences/CALS T&R Facultyen
pubs.organisational-group/Virginia Tech/All T&R Facultyen
pubs.organisational-group/Virginia Tech/Faculty of Health Sciencesen

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