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Healing; Wounds and injuries; Cells--Motility; Vascular endothelial growth factors


Endothelial cell motility is central to several biological processes including angiogenesis during wound healing, reendothelialization of vessel walls after damage and neovascularization of tumors. However, control mechanisms that stimulate and inhibit cell movement are not known. Our objective is to understand the signals that initiate movement of endothelial cells. To examine these questions, we used an in vitro wound model of quiescent pulmonary artery endothelial cell monolayers which were stimulated to move by mechanical injury. Ca2+ signaling at the time of wounding produces long lasting effects on cell movement. We investigated whether new gene transcription after wounding might also stimulate endothelial cell movement. Specifically, we examined transcriptional activation of vascular endothelial cell growth factor (VEGF) after injury. While many studies have reported that tumor and epithelial cells produce VEGF, there is conflicting evidence for VEGF synthesis by endothelial cells. We found that RNA transcripts for 121 and 165 amino acids VEGF isoforms were expressed in quiescent endothelial cells. These transcripts were also produced by ovarian cancer cells which induce angiogenesis in vivo. Surprisingly, after wounding, additional RNA transcripts encoding the 189 amino acid VEGF isoform were induced. VEGF might self-stimulate endothelial cells since exogenous, recombinant VEGF accelerated cell motility as much as basic fibroblast growth factor. Our data suggest that expression of the 189 amino acid VEGF isoform is upregulated in response to extravascular signals such as mechanical wounding. VEGF might act in an autocrine or paracrine manner to stimulate movement after wounding.

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