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2015 ; 2015
(ä): 391043
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WNT/?-Catenin Signaling Is Required for Integration of CD24+ Renal Progenitor
Cells into Glycerol-Damaged Adult Renal Tubules
#MMPMID26089915
Zhang Z
; Iglesias DM
; Corsini R
; Chu L
; Goodyer P
Stem Cells Int
2015[]; 2015
(ä): 391043
PMID26089915
show ga
During development, nephron progenitor cells (NPC) are induced to differentiate
by WNT9b signals from the ureteric bud. Although nephrogenesis ends in the
perinatal period, acute kidney injury (AKI) elicits repopulation of damaged
nephrons. Interestingly, embryonic NPC infused into adult mice with AKI are
incorporated into regenerating tubules. Since WNT/?-catenin signaling is crucial
for primary nephrogenesis, we reasoned that it might also be needed for the
endogenous repair mechanism and for integration of exogenous NPC. When we
examined glycerol-induced AKI in adult mice bearing a ?-catenin/TCF reporter
transgene, endogenous tubular cells reexpressed the NPC marker, CD24, and showed
widespread ?-catenin/TCF signaling. We isolated CD24+ cells from E15 kidneys of
mice with the canonical WNT signaling reporter. 40% of cells responded to WNT3a
in vitro and when infused into glycerol-injured adult, the cells exhibited
?-catenin/TCF reporter activity when integrated into damaged tubules. When
embryonic CD24+ cells were treated with a ?-catenin/TCF pathway inhibitor (IWR-1)
prior to infusion into glycerol-injured mice, tubular integration of cells was
sharply reduced. Thus, the endogenous canonical ?-catenin/TCF pathway is
reactivated during recovery from AKI and is required for integration of exogenous
embryonic renal progenitor cells into damaged tubules. These events appear to
recapitulate the WNT-dependent inductive process which drives primary
nephrogenesis.
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