Key result
Skeletal muscle-derived extract stimulates dose-dependent angiogenesis versus control.
Why the study?
The stimulus for vascular ingrowth into damaged skeletal muscle during regeneration is currently unknown.
Does skeletal muscle-derived extract stimulate neovascularization in a rabbit corneal assay?
Does skeletal muscle-derived extract stimulate neovascularization in a rabbit corneal assay?
Extracts from skeletal muscle contain factors capable of stimulating dose-dependent neovascularization, suggesting a mechanism for spontaneous blood vessel growth following muscle damage.
Muscle extract may stimulate post-injury revascularization; leaves open the factor's identity and any clinical role.
After a muscle is damaged, blood vessels spontaneously grow into the injured region as the muscle fibers regenerate. The stimulus for this vascular ingrowth is currently unknown. We hypothesized that the damaged muscle releases a factor(s) capable of stimulating this revascularization. To test this theory, extracts were prepared from rabbit hind limb muscles and incorporated into Hydron, a slow-release polymer. Pellets of the extract containing Hydron were implanted between the layers of the rabbit corneal stroma as an assay for angiogenic activity. The normally avascular corneas were examined 7 days after surgery for the presence of new blood vessels. Skeletal muscle-derived extract from rabbits elicited positive angiogenic responses in a dose-dependent manner. Four hundred to 500 micrograms of the skeletal muscle-derived extract were required to produce maximum vessel ingrowth. The control, Dulbecco's phosphate-buffered saline in Hydron, failed to stimulate neovascularization.
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Phillips et al. (1990) studied Damaged skeletal muscle. Skeletal muscle-derived extract in Hydron vs. Dulbecco's phosphate-buffered saline in Hydron was evaluated on Presence of new blood vessels (angiogenic response) in the corneal stroma. Skeletal muscle-derived extract from rabbits elicited positive angiogenic responses in a dose-dependent manner, whereas the control failed to stimulate neovascularization.
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