| First Author | Pullar CE | Year | 2012 |
| Journal | J Invest Dermatol | Volume | 132 |
| Issue | 8 | Pages | 2076-84 |
| PubMed ID | 22495178 | Mgi Jnum | J:189440 |
| Mgi Id | MGI:5445819 | Doi | 10.1038/jid.2012.108 |
| Citation | Pullar CE, et al. (2012) beta2AR antagonists and beta2AR gene deletion both promote skin wound repair processes. J Invest Dermatol 132(8):2076-84 |
| abstractText | 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 beta-adrenergic receptor autocrine/paracrine network exists in skin, but the role of beta2-adrenergic receptor (beta2AR) 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 beta2AR knockout excisional skin wound models) models were used to demonstrate that blockade or loss of beta2AR gene deletion promoted wound repair, a finding that is, to our knowledge, previously unreported. Compared with vehicle-only controls, beta2AR antagonism increased angiogenesis, dermal fibroblast function, and re-epithelialization, but had no effect on wound inflammation in vivo. Skin wounds in beta2AR knockout mice contracted and re-epithelialized faster in the first few days of wound repair in vivo. beta2AR antagonism enhanced cell motility through distinct intracellular signalling mechanisms and increased vascular endothelial growth factor secretion from keratinocytes. beta2AR antagonism promoted wound repair processes in the early stages of wound repair, revealing a possible new avenue for therapeutic intervention. |
