Relaxin induces vascular endothelial growth factor expression and angiogenesis selectively at wound sites

Relaxin is a reproductive hormone that has historically been characterized as being responsible for pubic ligament loosening and cervical ripening. Recently, relaxin has been associated with neovascularization of the endometrial lining of the uterus, potentially via specific induction of vascular en...

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Published in:Wound repair and regeneration 2000-09, Vol.8 (5), p.361-370
Main Authors: UNEMORI, ELAINE N, LEWIS, MARTYN, CONSTANT, JAMES, ARNOLD, GRETCHEN, GROVE, BEVERLY H, NORMAND, JOSEE, DESHPANDE, USHA, SALLES, ADAM, PICKFORD, LESLEY B, ERIKSON, MARK E, HUNT, THOMAS K, HUANG, XINFAN
Format: Article
Language:English
Subjects:
Animals
Cell Line
Cytokines - drug effects
Cytokines - genetics
Cytokines - secretion
Disease Models, Animal
Drug Evaluation, Preclinical
Endothelial Growth Factors - genetics
Endothelial Growth Factors - secretion
Fibroblast Growth Factor 2 - drug effects
Fibroblast Growth Factor 2 - genetics
Fibroblast Growth Factor 2 - secretion
Gene Expression - drug effects
Ischemia - complications
Ischemia - drug therapy
Lymphokines - drug effects
Lymphokines - genetics
Lymphokines - secretion
Macrophages - drug effects
Neovascularization, Physiologic - drug effects
Relaxin - pharmacology
Reverse Transcriptase Polymerase Chain Reaction
Transcription, Genetic
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Wound Healing - drug effects
Wounds and Injuries - complications
Wounds and Injuries - drug therapy
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Summary:Relaxin is a reproductive hormone that has historically been characterized as being responsible for pubic ligament loosening and cervical ripening. Recently, relaxin has been associated with neovascularization of the endometrial lining of the uterus, potentially via specific induction of vascular endothelial growth factor. Previously conducted clinical studies using partially purified porcine relaxin have described relaxin's ability to stimulate the healing of ischemic wounds, suggesting that relaxin may also have angiogenic effects at sites of ischemic wound healing. In the present study, relaxin's angiogenic effects in the context of wound repair were tested in rodent models of angiogenesis and wound healing. Relaxin showed an ability to stimulate new blood vessel formation, particularly at ischemic wound sites, and to induce both vascular endothelial growth factor and basic fibroblast growth factor specifically in cells, presumably including macrophages, collected from wound sites. Resident macrophages collected from nonwound sites, such as the lung, did not show altered expression of these cytokines following relaxin administration. Because angiogenic wound cells are frequently macrophages, THP‐1 cells, a cell line of monocyte lineage that binds relaxin specifically, were tested for and shown to induce vascular endothelial growth factor and basic fibroblast growth factor in response to relaxin. In conclusion, relaxin may be useful in the treatment of ischemic wounds by stimulating angiogenesis via the induction of vascular endothelial growth factor and basic fibroblast growth factor in wound macrophages.
ISSN:1067-1927
1524-475X
DOI:10.1111/j.1524-475X.2000.00361.x