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首页> 外文期刊>Molecular and Cellular Biology >Deletion of Vascular Endothelial Growth Factor C (VEGF-C) and VEGF-D Is Not Equivalent to VEGF Receptor 3 Deletion in Mouse Embryos
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Deletion of Vascular Endothelial Growth Factor C (VEGF-C) and VEGF-D Is Not Equivalent to VEGF Receptor 3 Deletion in Mouse Embryos

机译：小鼠胚胎中血管内皮生长因子C（VEGF-C）和VEGF-D的缺失不等同于VEGF受体3的缺失

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Lymphatic vessels play an important role in the regulation of tissue fluid balance, immune responses, and fat adsorption and are involved in diseases including lymphedema and tumor metastasis. Vascular endothelial growth factor (VEGF) receptor 3 (VEGFR-3) is necessary for development of the blood vasculature during early embryogenesis, but later, VEGFR-3 expression becomes restricted to the lymphatic vasculature. We analyzed mice deficient in both of the known VEGFR-3 ligands, VEGF-C and VEGF-D. Unlike the Vegfr3?/? embryos, the Vegfc?/?; Vegfd?/? embryos displayed normal blood vasculature after embryonic day 9.5. Deletion of Vegfr3 in the epiblast, using keratin 19 (K19) Cre, resulted in a phenotype identical to that of the Vegfr3?/? embryos, suggesting that this phenotype is due to defects in the embryo proper and not in placental development. Interestingly, the Vegfr3neo hypomorphic mutant mice carrying the neomycin cassette between exons 1 and 2 showed defective lymphatic development. Overexpression of human or mouse VEGF-D in the skin, under the K14 promoter, rescued the lymphatic hypoplasia of the Vegfc+/? mice in the K14-VEGF-D; Vegfc+/? compound mice, suggesting that VEGF-D is functionally redundant with VEGF-C in the stimulation of developmental lymphangiogenesis. Our results suggest VEGF-C- and VEGF-D-independent functions for VEGFR-3 in the early embryo.
机译：淋巴管在调节组织液平衡，免疫反应和脂肪吸收中起重要作用，并参与包括淋巴水肿和肿瘤转移在内的疾病。血管内皮生长因子（VEGF）受体3（VEGFR-3）是早期胚胎发生过程中血管系统发育所必需的，但是后来，VEGFR-3的表达就局限于淋巴管系统。我们分析了缺乏两种已知的VEGFR-3配体，VEGF-C和VEGF-D的小鼠。与 Vegfr3 ？/？胚胎不同， Vegfc ？/？;胚胎第9.5天后， Vegfd ？/？胚胎显示出正常的血管。使用角蛋白19（K19）Cre删除表皮细胞中的 Vegfr3 ，其表型与 Vegfr3 ？/？胚胎的表型相同，表明该表型是由于胚胎固有缺陷而不是胎盘发育所致。有趣的是，在外显子1和2之间携带新霉素盒的 Vegfr3 neo 亚型突变小鼠表现出有缺陷的淋巴发育。在K14启动子的作用下，人或小鼠VEGF-D在皮肤中的过表达可以挽救 Vegfc + /？小鼠在K14-VEGF-D中的淋巴发育不良。 Vegfc + /？复合小鼠，提示VEGF-D在刺激发育性淋巴管生成中与VEGF-C在功能上是多余的。我们的结果表明，早期胚胎中VEGFR-3的VEGF-C-和VEGF-D独立功能。

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