肾单位
硫氧化物9
急性肾损伤
肾
再生(生物学)
下调和上调
肾干细胞
医学
细胞生物学
癌症研究
生物
内科学
干细胞
基因表达
基因
祖细胞
生物化学
作者
Sanjeev Kumar,Jing Liu,Paul Pang,A. Michaela Krautzberger,Antoine Reginensi,Haruhiko Akiyama,Andreas Schedl,Benjamin D. Humphreys,Andrew P. McMahon
出处
期刊:Cell Reports
[Elsevier]
日期:2015-08-01
卷期号:12 (8): 1325-1338
被引量:169
标识
DOI:10.1016/j.celrep.2015.07.034
摘要
After acute kidney injury (AKI), surviving cells within the nephron proliferate and repair. We identify Sox9 as an acute epithelial stress response in renal regeneration. Translational profiling after AKI revealed a rapid upregulation of Sox9 within proximal tubule (PT) cells, the nephron cell type most vulnerable to AKI. Descendants of Sox9(+) cells generate the bulk of the nephron during development and regenerate functional PT epithelium after AKI-induced reactivation of Sox9 after renal injury. After restoration of renal function post-AKI, persistent Sox9 expression highlights regions of unresolved damage within injured nephrons. Inactivation of Sox9 in PT cells pre-injury indicates that Sox9 is required for the normal course of post-AKI recovery. These findings link Sox9 to cell intrinsic mechanisms regulating development and repair of the mammalian nephron.
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