Polyclonal antibodies directed against human recombinant basic fibroblast growth factor (bFGF) were used in immunohistochemical studies to localize this growth factor in normal and wounded rat skeletal muscles. bFGF i...Polyclonal antibodies directed against human recombinant basic fibroblast growth factor (bFGF) were used in immunohistochemical studies to localize this growth factor in normal and wounded rat skeletal muscles. bFGF immunoreactivity was found mainly in the extracellular matrix, primarily in the endomysium, including 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. After 4-hour ischemia, about 40% of skeletal muscle fibers lost their bFGF immunoreactivity. Muscles which experienced 4-hour ischemia and 24 reperfusion had only a weaker bFGF immunoreactivity. The pathological results supported the concept of destroyed cell connection and fiber necrosis in ischemia and reperfused muscles. The mechanisms involved in this reduced concentration of bFGF in wounded muscles included oxygen radical activation, inflammatory response and reduced secretion of endogenous bFGF. These results were only partially compatible with the established mitogenic role of this protein and suggested that a reduction of endogenous FGF may partly contribute to a delay in wound healing.展开更多
文摘Polyclonal antibodies directed against human recombinant basic fibroblast growth factor (bFGF) were used in immunohistochemical studies to localize this growth factor in normal and wounded rat skeletal muscles. bFGF immunoreactivity was found mainly in the extracellular matrix, primarily in the endomysium, including 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. After 4-hour ischemia, about 40% of skeletal muscle fibers lost their bFGF immunoreactivity. Muscles which experienced 4-hour ischemia and 24 reperfusion had only a weaker bFGF immunoreactivity. The pathological results supported the concept of destroyed cell connection and fiber necrosis in ischemia and reperfused muscles. The mechanisms involved in this reduced concentration of bFGF in wounded muscles included oxygen radical activation, inflammatory response and reduced secretion of endogenous bFGF. These results were only partially compatible with the established mitogenic role of this protein and suggested that a reduction of endogenous FGF may partly contribute to a delay in wound healing.
