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Ischemia and reperfusion reduce the endogenous basic fibroblast growth factor in rat skeletal muscles: An immunohistochemical study

AutorFu, X.; Cuevas, Pedro; Giménez-Gallego, Guillermo ; Martínez-Murillo, Ricardo ; Tian, H.; Sheng, Z.
Palabras claveFibroblast growth Factor immuno-reactivity Factor immunoreactivity
Fecha de publicación1996
EditorBlackwell Publishing
CitaciónWound Repair and Regeneration 4: 381- 385 (1996)
ResumenPolyclonal antibodies directed against human recombinant basic fibroblast growth factor were used in immunohistochemical studies to localize this growth factor in normal and wounded rat skeletal muscles. According to the intensity of the stain, three main classes of fibers could be identified: the strongly, moderately, and weakly stained fibers. Basic fibrobiast growth factor immunoreactivity was found mainly in the extracellular matrix primarily in the endomysium, which includes the heparin-containing basal lamina and also in the capillary basal membrane of both normal and wounded muscles; however, the signal intensity was much stronger in normal muscles. The distribution of basic fibroblast growth factor in wounded muscles became markedly heterogeneous and sparse. After 4 hours of ischemia about 40% of skeletal muscle fibers lost their basic fibroblast growth factor immuno-reactivity. Muscles which underwent 4 hours of ischemia and 24 hours of reperfusion had only a diminished basic fibroblast growth factor immunoreactivity. The pathologic results supported the concept of destroyed cell connection and fiber necrosis in ischemic and reperfused muscles. Potential mechanisms involved in this reduced concentration of basic fibroblast growth factor in wounded muscles may include oxygen free radical activation, a generalized effect of the inflammatory response, and reduced secretion of endogenous basic fibroblast growth factor. These results are only partially compatible with the established mitogenic role of this growth factor and suggest that a reduction of endogenous fibroblast growth factor may partly contribute to a delay in wound healing. Copyright © 1996 by The Wound Healing Society.
URIhttp://hdl.handle.net/10261/155415
DOInull
Identificadoresdoi: null
issn: 1067-1927
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