VEGF-induced angiogenesis and scar formation

描述（由申请人提供）：在发育的前两个三个月期间，胎儿以无疤痕的方式愈合皮肤伤口，这是一个非常迅速且无炎症的过程。相比之下，从发育的第三个三个月到成年期的皮肤愈合更慢，包括显著的炎症阶段，并导致形成永久性疤痕。虽然成人伤口修复表现出一个强大的时期的血管生成，伤口血管生成还没有很好地描述在无瘢痕胎儿愈合。我们的初步数据表明无瘢痕胎儿伤口血管生成水平降低。拟议的研究将检查伤口血管生成对胎儿和成人皮肤瘢痕形成的贡献。我们将描述伤口血管生成和促血管生成分子血管内皮生长因子（VEGF）及其受体在胎儿伤口修复中的生产模式。此外，我们将使用无瘢痕胎儿愈合和成人伤口修复的小鼠模型来研究VEGF诱导的血管生成对瘢痕形成的影响。更好地了解胎儿皮肤中发生的无瘢痕愈合过程可能会导致识别用于增强产后修复结果的治疗靶点。

DESCRIPTION (provided by applicant): During the first two trimesters of development, the fetus heals skin wounds in a scarless manner, a process that occurs very rapidly and without inflammation. In contrast, skin beyond the third trimester of development through adulthood heals more slowly, includes a significant inflammatory phase, and results in the formation of a permanent scar. Although adult wound repair exhibits a robust period of angiogenesis, wound angiogenesis has not been well described in scarless fetal healing. Our preliminary data suggests reduced levels of angiogenesis in scarless fetal wounds. The proposed studies will examine the contribution of wound angiogenesis to scar formation in fetal and adult skin. We will characterize wound angiogenesis and the production pattern of the pro-angiogenic molecule vascular endothelial growth factor (VEGF) and its receptors in fetal wound repair. In addition, we will examine the effects of VEGF-induced angiogenesis on scar formation using murine models of scarless fetal healing and adult wound repair. A better understanding of the scarless healing process that occurs in fetal skin could lead to the identification of therapeutic targets used to enhance the outcome of postnatal repair.