Journal
PHARMACOLOGICAL RESEARCH
Volume 58, Issue 2, Pages 158-164Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2008.07.012
Keywords
Wound healing; beta-Adrenergic receptor; Inflammation; Angiogenesis; Keratinocyte migration; Re-epithelialization; Angiogenesis; Dermal fibroblast; Wound contraction
Categories
Funding
- Wellcome Trust
- British Skin Foundation
- School of Medicine, University of California, Davis
- University of California, Davis [UL1 RR024146]
- National Center for Research Resources (NCRR)
- National Institutes of Health (NIH)
- Shriners Hospitals for Children and the Veterans Administration
Ask authors/readers for more resources
Adrenergic receptors and their downstream effector molecules are expressed in all cell types in the skin, and it is only recently that functionality of the catecholamine agonist activated signaling in the cutaneous repair process has been revealed. In addition to responding to systemic elevations in catecholamines (as in stress situations) or to pharmacologically administered adrenergic agonists, epidermal keratinocytes themselves can synthesize catecholamine ligands. They also respond to these systemic or self-generated agonists via receptor mediated signaling, resulting in altered migration, and changes in wound re-epithelialization. Endothelial cells, inflammatory cells, dermal fibroblasts, and mesenchymal stem cells, all cells that contribute to the wound repair process, express multiple subtypes of adrenergic receptors and exhibit responses that can be either contribute or impair healing-and occasionally, depending on the species and assay conditions, results can be conflicting. There is still much to be uncovered regarding how this self-contained autocrine and paracrine signaling system contributes to cutaneous wound repair. (c) 2008 Published by Elsevier Ltd.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available