Division of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Division of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Cell Rep. 2019 Jan 29;26(5):1318-1332.e4. doi: 10.1016/j.celrep.2019.01.005.
Altered DNA methylation plays an important role in the onset and progression of kidney disease. However, little is known about how the changes arise in disease states. Here, we report that KAT5-mediated DNA damage repair is essential for the maintenance of kidney podocytes and is associated with DNA methylation status. Podocyte-specific KAT5-knockout mice develop severe albuminuria with increased DNA double-strand breaks (DSBs), increased DNA methylation of the nephrin promoter region, and decreased nephrin expression. Podocyte KAT5 expression is decreased, whereas DNA DSBs and DNA methylation are increased in diabetic nephropathy; moreover, KAT5 restoration by gene transfer attenuates albuminuria. Furthermore, KAT5 decreases DNA DSBs and DNA methylation at the same nephrin promoter region, which indicates that KAT5-mediated DNA repair may be related to DNA methylation status. These results suggest a concept in which an environment of DNA damage repair, which occurs with decreased KAT5, may affect DNA methylation status.
DNA 甲基化的改变在肾脏疾病的发生和进展中起着重要作用。然而,对于疾病状态下这些变化是如何产生的,人们知之甚少。在这里,我们报告说,KAT5 介导的 DNA 损伤修复对于维持肾脏足细胞是必不可少的,并且与 DNA 甲基化状态相关。足细胞特异性 KAT5 敲除小鼠发生严重的白蛋白尿,伴有 DNA 双链断裂 (DSB) 增加、nephrin 启动子区域的 DNA 甲基化增加和 nephrin 表达减少。在糖尿病肾病中,足细胞 KAT5 的表达减少,而 DNA DSB 和 DNA 甲基化增加;此外,通过基因转移恢复 KAT5 可减轻白蛋白尿。此外,KAT5 可降低同一 nephrin 启动子区域的 DNA DSB 和 DNA 甲基化,这表明 KAT5 介导的 DNA 修复可能与 DNA 甲基化状态有关。这些结果表明,在 KAT5 减少的情况下,DNA 损伤修复的环境可能会影响 DNA 甲基化状态。