Diabetes Increases Cryoinjury Size with Associated Effects on Cx43 Gap Junction Function and Phosphorylation in the Mouse Heart

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dc.contributor.authorPalatinus, Joseph A.en
dc.contributor.authorGourdie, Robert G.en
dc.contributor.departmentFralin Biomedical Research Instituteen
dc.contributor.departmentSchool of Biomedical Engineering and Sciencesen
dc.date.accessioned2017-02-14T17:08:24Zen
dc.date.available2017-02-14T17:08:24Zen
dc.date.issued2016en
dc.description.abstractDiabetic patients develop larger myocardial infarctions and have an increased risk of death following a heart attack. The poor response to myocardial injury in the diabetic heart is likely related to the many metabolic derangements from diabetes that create a poor substrate in general for wound healing, response to injury and infection. Studies in rodents have implicated a role for the gap junction protein connexin 43 (Cx43) in regulating the injury response in diabetic skin wounds. In this study, we sought to determine whether diabetes alters Cx43 molecular interactions or intracellular communication in the cryoinjured STZ type I diabetic mouse heart. We found that epicardial cryoinjury size is increased in diabetic mice and this increase is prevented by preinjury insulin administration. Consistent with these findings, we found that intercellular coupling via gap junctions is decreased after insulin administration in diabetic and nondiabetic mice. This decrease in coupling is associated with a concomitant increase in phosphorylation of Cx43 at serine 368, a residue known to decrease channel conductance. Taken together, our results suggest that insulin regulates both gap junction-mediated intercellular communication and injury propagation in the mouse heart.en
dc.description.versionPublished versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationJoseph A. Palatinus and Robert G. Gourdie, “Diabetes Increases Cryoinjury Size with Associated Effects on Cx43 Gap Junction Function and Phosphorylation in the Mouse Heart,” Journal of Diabetes Research, vol. 2016, Article ID 8789617, 9 pages, 2016. doi:10.1155/2016/8789617en
dc.identifier.doihttps://doi.org/10.1155/2016/8789617en
dc.identifier.eissn2314-6753en
dc.identifier.urihttp://hdl.handle.net/10919/75027en
dc.identifier.volume2016en
dc.language.isoenen
dc.relation.urihttp://www.ncbi.nlm.nih.gov/pubmed/27034963en
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.holderCopyright © 2016 Joseph A. Palatinus and Robert G. Gourdie. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectAnimalsen
dc.subjectCold Temperatureen
dc.subjectConnexin 43en
dc.subjectDiabetes Mellitus, Experimentalen
dc.subjectGap Junctionsen
dc.subjectHypoglycemic Agentsen
dc.subjectInsulinen
dc.subjectMice, Inbred C57BLen
dc.subjectMyocardial Infarctionen
dc.subjectMyocardiumen
dc.subjectPhosphorylationen
dc.subjectSignal Transductionen
dc.subjectStreptozocinen
dc.titleDiabetes Increases Cryoinjury Size with Associated Effects on Cx43 Gap Junction Function and Phosphorylation in the Mouse Hearten
dc.title.serialJournal of Diabetes Researchen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.otherResearch Support, N.I.H., Extramuralen
dc.type.otherResearch Support, Non-U.S. Gov'ten
pubs.organisational-group/Virginia Techen
pubs.organisational-group/Virginia Tech/All T&R Facultyen
pubs.organisational-group/Virginia Tech/Faculty of Health Sciencesen
pubs.organisational-group/Virginia Tech/University Research Institutesen
pubs.organisational-group/Virginia Tech/University Research Institutes/Virginia Tech Carilion Research Instituteen

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