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dc.contributor.authorMoore, Keithen
dc.contributor.authorGhatnekar, Gautam S.en
dc.contributor.authorGourdie, Robert G.en
dc.contributor.authorPotts, Jay D.en
dc.coverage.spatialUnited Statesen
dc.date.accessioned2017-02-09T20:20:02Zen
dc.date.available2017-02-09T20:20:02Zen
dc.date.issued2014en
dc.identifier.urihttp://hdl.handle.net/10919/74985en
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
dc.format.extente86570 - ? page(s)en
dc.languageengen
dc.relation.urihttp://www.ncbi.nlm.nih.gov/pubmed/24466155en
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectAnimalsen
dc.subjectBiomarkersen
dc.subjectBlotting, Westernen
dc.subjectCapsulesen
dc.subjectConnexin 43en
dc.subjectCorneal Diseasesen
dc.subjectDelayed-Action Preparationsen
dc.subjectDiabetes Mellitus, Experimentalen
dc.subjectDiabetes Mellitus, Type 1en
dc.subjectEnzyme-Linked Immunosorbent Assayen
dc.subjectEpithelial-Mesenchymal Transitionen
dc.subjectGlucose Transporter Type 4en
dc.subjectInflammationen
dc.subjectMaleen
dc.subjectPeptide Fragmentsen
dc.subjectRNA, Messengeren
dc.subjectRatsen
dc.subjectRats, Sprague-Dawleyen
dc.subjectReal-Time Polymerase Chain Reactionen
dc.subjectReverse Transcriptase Polymerase Chain Reactionen
dc.subjectWound Healingen
dc.titleImpact of the controlled release of a connexin 43 peptide on corneal wound closure in an STZ model of type I diabetes.en
dc.typeArticle - Refereeden
dc.description.versionPublished online (Publication status)en
dc.contributor.departmentBiomedical Engineering and Mechanicsen
dc.contributor.departmentFralin Biomedical Research Instituteen
dc.title.serialPLoS Oneen
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0086570en
dc.type.otherResearch Support, N.I.H., Extramuralen
dc.type.otherResearch Support, Non-U.S. Gov'ten
dc.identifier.volume9en
dc.identifier.issue1en
dc.identifier.eissn1932-6203en
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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