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首页> 外文期刊>Development >Met and the epidermal growth factor receptor act cooperatively to regulate final nephron number and maintain collecting duct morphology.
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Met and the epidermal growth factor receptor act cooperatively to regulate final nephron number and maintain collecting duct morphology.

机译：Met和表皮生长因子受体协同作用，以调节最终的肾单位并维持收集管的形态。

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摘要

Ureteric bud (UB) branching during kidney development determines the final number of nephrons. Although hepatocyte growth factor and its receptor Met have been shown to stimulate branching morphogenesis in explanted embryonic kidneys, loss of Met expression is lethal during early embryogenesis without obvious kidney abnormalities. Met(fl/fl);HoxB7-Cre mice, which lack Met expression selectively in the UB, were generated and found to have a reduction in final nephron number. These mice have increased Egf receptor expression in both the embryonic and adult kidney, and exogenous Egf can partially rescue the branching defect seen in kidney explants. Met(fl/fl);HoxB7-Cre;wa-2/wa-2 mice, which lack normal Egfr and Met signaling, exhibit small kidneys with a marked decrease in UB branching at E14.5 as well as a reduction in final glomerular number. These mice developed progressive interstitial fibrosis surrounding collecting ducts with kidney failure and death by 3-4 weeks of age. Thus, in support of previousin vitro findings, Met and the Egf receptor can act cooperatively to regulate UB branching and mediate maintenance of the normal adult collecting duct.
机译：肾脏发育过程中的输尿管芽（UB）分支决定了肾单位的最终数量。尽管已显示肝细胞生长因子及其受体Met可以刺激移植的胚胎肾脏中的分支形态发生，但Met表达的丧失在早期胚胎发生过程中是致命的，而没有明显的肾脏异常。生成了在UB中选择性缺乏Met表达的Met（fl / fl）; HoxB7-Cre小鼠，发现其最终肾单位数目减少。这些小鼠在胚胎和成年肾脏中都有增加的Egf受体表达，并且外源性Egf可以部分挽救在肾脏外植体中看到的分支缺陷。 Met（fl / fl）; HoxB7-Cre; wa-2 / wa-2小鼠缺乏正常的Egfr和Met信号传导，表现出小肾脏，在E14.5处的UB分支明显减少，并且最终肾小球减少数。这些小鼠到3-4周龄时，在收集管周围发生进行性间质纤维化，并伴有肾功能衰竭和死亡。因此，为支持先前的体外发现，Met和Egf受体可以协同作用来调节UB分支并介导正常成人收集管的维持。

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