期刊
JOURNAL OF SURGICAL RESEARCH
卷 135, 期 2, 页码 218-225出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.jss.2006.04.006
关键词
angiogenesis; regression; wound; VEGF; FGF; PDGF
类别
资金
- NIGMS NIH HHS [R01-GM50875, T32-GM08750, R01-GM55238, R01 GM050875] Funding Source: Medline
Background. In healing wounds, rising levels of vascular endothelial growth factor (VEGF) induce a period of robust angiogenesis. The levels of proangiogenic factors in the wound begin to decline just before a period of vascular regression, suggesting that these mediators are necessary to sustain vessel density. The purpose of this study was to determine if the maintenance of pro-angiogenic stimuli in the wound would prevent physiological vessel regression. Materials and methods. A standard subcutaneous sponge wound model was modified by the addition of a mini-osmotic pump, allowing manipulation of the wound milieu by the addition of exogenous growth factors. After initial characterization of this model, exogenous VEGF (10 mu g/mL), FGF (10 mu g/mL), PDGF (10 mu g/mL), or VEGF (10 mu g/mL) plus FGF (10 mu g/mL) were delivered to wounds and blood vessel density analyzed by immunohistochemistry. Results. VEGF administration resulted in a transient increase in wound vessel density (P < 0.05). None of the pro-angiogenic growth factors (VEGF, FGF, PDGF, VEGF/FGF) were able to prevent vascular regression (P = NS). Conclusions. These findings suggest that the antiangiogenic signals that mediate physiological vascular regression in wounds are strongly dominant over pro-angiogenic stimuli during the later phases of wound healing. Clinical manipulation of anti-angiogenic signals in addition to the currently used pro-angiogenic targets may be needed to achieve therapeutic modulation of blood vessel density. (c) 2006 Elsevier Inc. All rights reserved.
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