Journal
CELL REPORTS
Volume 12, Issue 8, Pages 1325-1338Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.07.034
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Funding
- John McKay Fellowship Award from University Kidney Research Organisation, Los Angeles
- Agence Nationale de la Recherche [09-Geno-027-01, ANR-11-LABX-0028-01]
- Fondation Recherche Medicale
- California Institute for Regenerative Medicine [LA1-06536]
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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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