Roles of Foxc transcription factors in podocyte injury.

本项目旨在阐明Foxc1和Foxc2在肾脏发育和肾小球硬化发生中的作用。携带零突变Foxc1基因的小鼠经常由于异位出芽而产生异常的双收集系统。然而，异位出芽本身并不会导致肾脏发育不良。令人感兴趣的是，Foxc1的表达并不影响其表达的后肾间质的命运，而是通过Wolffian导管控制芽形成的部位。我们正在分析Foxc2缺失小鼠的肾脏组织，Foxc1敲除小鼠的足细胞特异性。我们还生成了Foxc2 loxP小鼠，使我们能够生成肾脏特异性Foxc2条件敲除小鼠。

This project is aimed to clarify roles of Foxc1 and Foxc2 in the kidney development and the development of glomerular sclerosis. Mice carrying null mutated Foxc1 gene frequently develop anomalous double collecting system due to ectopic budding. However, ectopic budding per se does not contribute to kidney dysplasia. It is intriguing that Foxc1 expression does not affect the fate of metanephric mesenchyme where it is expressed but controls the site of bud formation by the Wolffian duct. We are analyzing kidney tissues from Foxc2 null mice, podocyte specific Foxc1 knockoutmice. We also generated Foxc2 loxP mice that enable us to generate kidney specific Foxc2 conditional knockout mice.