Sox9 Activation Highlights a Cellular Pathway of Renal Repair in the Acutely Injured Mammalian Kidney

Sanjeev Kumar, Jing Liu, Paul Pang, A. Michaela Krautzberger, Antoine Reginensi, Haruhiko Akiyama, Andreas Schedl, Benjamin D. Humphreys, Andrew P. McMahon

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67 Scopus citations

Abstract

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.

Original languageEnglish
Article number1940
Pages (from-to)1325-1338
Number of pages14
JournalCell Reports
Volume12
Issue number8
DOIs
StatePublished - Aug 25 2015
Externally publishedYes

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    Kumar, S., Liu, J., Pang, P., Krautzberger, A. M., Reginensi, A., Akiyama, H., Schedl, A., Humphreys, B. D., & McMahon, A. P. (2015). Sox9 Activation Highlights a Cellular Pathway of Renal Repair in the Acutely Injured Mammalian Kidney. Cell Reports, 12(8), 1325-1338. [1940]. https://doi.org/10.1016/j.celrep.2015.07.034