β2AR antagonists and Β2AR gene deletion both promote skin wound repair processes

Christine E. Pullar, Gabrielle S. Le Provost, Andrew P. O'Leary, Sian E. Evans, Brian S. Baier, Roslyn Rivkah Isseroff

Research output: Contribution to journalArticle

41 Scopus citations

Abstract

Skin wound healing is a complex process requiring the coordinated, temporal orchestration of numerous cell types and biological processes to regenerate damaged tissue. Previous work has demonstrated that a functional Β-adrenergic receptor autocrine/paracrine network exists in skin, but the role of Β2-adrenergic receptor (Β2AR) in wound healing is unknown. A range of in vitro (single-cell migration, immunoblotting, ELISA, enzyme immunoassay), ex vivo (rat aortic ring assay), and in vivo (chick chorioallantoic membrane assay, zebrafish, murine wild-type, and Β2AR knockout excisional skin wound models) models were used to demonstrate that blockade or loss of Β2AR gene deletion promoted wound repair, a finding that is, to our knowledge, previously unreported. Compared with vehicle-only controls, Β2AR antagonism increased angiogenesis, dermal fibroblast function, and re-epithelialization, but had no effect on wound inflammation in vivo. Skin wounds in Β2AR knockout mice contracted and re-epithelialized faster in the first few days of wound repair in vivo. Β2AR antagonism enhanced cell motility through distinct intracellular signalling mechanisms and increased vascular endothelial growth factor secretion from keratinocytes. Β2AR antagonism promoted wound repair processes in the early stages of wound repair, revealing a possible new avenue for therapeutic intervention.

Original languageEnglish (US)
Pages (from-to)2076-2084
Number of pages9
JournalJournal of Investigative Dermatology
Volume132
Issue number8
DOIs
StatePublished - Aug 2012

ASJC Scopus subject areas

  • Dermatology
  • Biochemistry
  • Cell Biology
  • Molecular Biology

Fingerprint Dive into the research topics of 'β2AR antagonists and Β2AR gene deletion both promote skin wound repair processes'. Together they form a unique fingerprint.

  • Cite this