Connexin 43 Antisense Therapy Modulates Connexin Expression and Wound Repair in Nitrogen Mustard Injured Mouse Skin

Published on Apr 1, 2015in The FASEB Journal4.966
路 DOI :10.1096/FASEBJ.29.1_SUPPLEMENT.876.3
Yoke-Chen Chang7
Estimated H-index: 7
(RU: Rutgers University),
Hui-Ying Chang2
Estimated H-index: 2
(RU: Rutgers University)
+ 4 AuthorsDonald R. Gerecke18
Estimated H-index: 18
(RU: Rutgers University)
Connexin 43 (Cx43) antisense treatment accelerates diabetic skin wound repair. Cx43 expression and its phosphorylation (pCx43) alters gap junction communication during skin wound repair. Vesicant induced skin injury results in prolonged wound healing similar to diabetic wounds. We performed a time course study using Cx43 antisense oligodeoxynucleotides (asODN) on nitrogen mustard (NM) injured SKH-1 hairless mouse dorsal skin to evaluate wound progression and Cx expression. Immunofluorescent (IF) analysis of NM injured skin demonstrated increased keratin 17 (K17, skin wound marker), increased expression of Cx26 and pCx43, and minimal expression of Cx43 by day 1. All markers were up-regulated with time as the wounds progressed. Dual-labeling studies indicated strong expression of Cx26 near the leading edge of wounds. In contrast, Cx43 and pCx43 were highly expressed in the hyperplastic epithelium. Cx43asODN treatment improved NM wounded skin as indicated by minimal K17 expression at day 1. Western blotting ...
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Systemic administration of a Connexin43 mimetic peptide, Peptide5, has been shown to reduce secondary tissue damage and improve functional recovery after spinal cord injury (SCI). This study investigated safety measures and potential off-target effects of Peptide5 systemic administration. Rats were subjected to a mild contusion SCI using the New York University impactor. One cohort was injected intraperitoneally with a single dose of fluorescently labelled Peptide5 and euthanised at 2 or 4 h pos...
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