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dc.contributor.authorMoore, Keithen_US
dc.contributor.authorGhatnekar, Gautam S.en_US
dc.contributor.authorGourdie, Robert G.en_US
dc.contributor.authorPotts, Jay D.en_US
dc.coverage.spatialUnited Statesen_US
dc.date.accessioned2017-02-09T20:20:02Z
dc.date.available2017-02-09T20:20:02Z
dc.date.issued2014en_US
dc.identifier.urihttp://hdl.handle.net/10919/74985
dc.description.abstractThe alpha-carboxy terminus 1 (αCT1) peptide is a synthetically produced mimetic modified from the DDLEI C-terminus sequence of connexin 43 (Cx43). Previous research using various wound healing models have found promising therapeutic effects when applying the drug, resulting in increased wound healing rates and reduced scarring. Previous data suggested a rapid metabolism rate in vitro, creating an interest in long term release. Using a streptozotocin (STZ) type I diabetic rat model with a surgically induced corneal injury, we delivered αCT1 both directly, in a pluronic gel solution, and in a sustained system, using polymeric alginate-poly-l-ornithine (A-PLO) microcapsules (MC). Fluorescent staining of wound area over a 5 day period indicated a significant increase in wound closure rates for both αCT1 and αCT1 MC treated groups, withαCT1 MC groups showing the most rapid wound closure overall. Analysis of inflammatory reaction to the treatment groups indicated significantly lower levels of both Interferon Inducible T-Cell Alpha Chemoattractant (ITAC) and Tumor Necrosis Factor Alpha (TNFα) markers using confocal quantification and ELISA assays. Additional analysis examining genes selected from the EMT pathway using RT-PCR and Western blotting suggested αCT1 modification of Transforming Growth Factor Beta 2 (TGFβ2), Keratin 8 (Krt8), Estrogen Receptor 1 (Esr1), and Glucose Transporter 4 (Glut4) over a 14 day period. Combined, this data indicated a possible suppression of the inflammatory response by αCT1, leading to increased wound healing rates.en_US
dc.format.extente86570 - ? page(s)en_US
dc.languageengen_US
dc.relation.urihttp://www.ncbi.nlm.nih.gov/pubmed/24466155en_US
dc.subjectAnimalsen_US
dc.subjectBiomarkersen_US
dc.subjectBlotting, Westernen_US
dc.subjectCapsulesen_US
dc.subjectConnexin 43en_US
dc.subjectCorneal Diseasesen_US
dc.subjectDelayed-Action Preparationsen_US
dc.subjectDiabetes Mellitus, Experimentalen_US
dc.subjectDiabetes Mellitus, Type 1en_US
dc.subjectEnzyme-Linked Immunosorbent Assayen_US
dc.subjectEpithelial-Mesenchymal Transitionen_US
dc.subjectGlucose Transporter Type 4en_US
dc.subjectInflammationen_US
dc.subjectMaleen_US
dc.subjectPeptide Fragmentsen_US
dc.subjectRNA, Messengeren_US
dc.subjectRatsen_US
dc.subjectRats, Sprague-Dawleyen_US
dc.subjectReal-Time Polymerase Chain Reactionen_US
dc.subjectReverse Transcriptase Polymerase Chain Reactionen_US
dc.subjectWound Healingen_US
dc.titleImpact of the controlled release of a connexin 43 peptide on corneal wound closure in an STZ model of type I diabetes.en_US
dc.typeArticle - Refereed
dc.description.versionPublished online (Publication status)en_US
dc.title.serialPLoS Oneen_US
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0086570
dc.type.otherResearch Support, N.I.H., Extramuralen_US
dc.type.otherResearch Support, Non-U.S. Gov'ten_US
dc.identifier.volume9en_US
dc.identifier.issue1en_US
dc.identifier.eissn1932-6203en_US
pubs.organisational-group/Virginia Tech
pubs.organisational-group/Virginia Tech/All T&R Faculty
pubs.organisational-group/Virginia Tech/Faculty of Health Sciences
pubs.organisational-group/Virginia Tech/University Research Institutes
pubs.organisational-group/Virginia Tech/University Research Institutes/Virginia Tech Carilion Research Institute


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