Biomolecular approach for the optimal flap surgery

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In order to further obtain the molecular mechanisms of the optimal flap survival, the signal transduction pathways of the cytokines were primarily investigate. In the primary culture model for human keloid-derived fibroblasts, Insulin-like Growth Factor-1 and its receptor involved in the keloid-derived fibroblasts resistance against the ceramide-induced apoptosis, therefore they are concluded as the primary cause of the cellar hyper-expression and the possible excessive production of the extracelluar matrix seen in keloid patients. In the further experiment, the axial-pattern epigastric flap was adopted as the flap survival model. In the modified epigastric flap, the cytokine-dependent gp130 receptor submit was strongly attributed to the flap survival, the pedicle blood flow, the microangiography and the angiogenesis transcript expression represented By VEGF. Therefore, the cytokine signaling via receptor was the major component for the flap angiogenesis as well as the flap blood flow.