Nature Medicine
1, 453 - 459 (1995)
doi:10.1038/nm0595-453
Ischaemia-induced expression of bFGF in normal skeletal muscle: A potential paracrine mechanism for mediating angiogenesis in ischaemic skeletal muscleKlaus J. Walgenbach1, Catherine Gratas2, Kenneth C. Shestak1
& Dorothea Becker2, 3
1Department of Surgery, Division of Plastic Surgery, 211 Lothrop Street, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA
2Department of Medicine, 211 Lothrop Street, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA
3Correspondence should be addressed to D.B. To test the hypothesis that induction of endogenous bFGF can lead to angiogenesis in ischaemic skeletal muscle, we studied the expression of bFGF after transposition of a well-vascularized muscle flap onto an ischaemic hindlimb in the rabbit. The results indicated a marked induction of bFGF mRNA throughout the myoblasts of the well-perfused muscle flap but not the myoblasts of the ischaemic muscle. bFGF protein was detected in the muscle flap, particularly in the myoblasts located closest to a newly formed, adjacent interface, and in the interface itself. In contrast, bFGF expression was not induced after transposition of a well-perfused muscle flap onto healthy muscle tissue. These data provide evidence that the juxtaposition of ischaemic skeletal muscle with healthy mesenchymal tissue triggers an increased expression of bFGF in the myoblasts of the well-perfused muscle. This paracrine induction of bFGF, in turn, leads to increased angiogenesis and regeneration of the ischaemic skeletal muscle.
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