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2015 ; 5
(ä): 7695
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Palladin is upregulated in kidney disease and contributes to epithelial cell
migration after injury
#MMPMID25573828
Chang EH
; Gasim AH
; Kerber ML
; Patel JB
; Glaubiger SA
; Falk RJ
; Jennette JC
; Otey CA
Sci Rep
2015[Jan]; 5
(ä): 7695
PMID25573828
show ga
Recovery from acute kidney injury involving tubular epithelial cells requires
proliferation and migration of healthy cells to the area of injury. In this
study, we show that palladin, a previously characterized cytoskeletal protein, is
upregulated in injured tubules and suggest that one of its functions during
repair is to facilitate migration of remaining cells to the affected site. In a
mouse model of anti-neutrophilic cytoplasmic antibody involving both tubular and
glomerular disease, palladin is upregulated in injured tubular cells, crescents
and capillary cells with angiitis. In human biopsies of kidneys from patients
with other kidney diseases, palladin is also upregulated in crescents and injured
tubules. In LLC-PK1 cells, a porcine proximal tubule cell line, stress induced by
transforming growth factor-?1 (TGF-?1) leads to palladin upregulation. Knockdown
of palladin in LLC-PK1 does not disrupt cell morphology but does lead to a defect
in cell migration. Furthermore, TGF-?1 induced increase in the 75 kDa palladin
isoform occurs in both the nucleus and the cytoplasm. These data suggest that
palladin expression is induced in injured cells and contributes to proper
migration of cells in proximal tubules, possibly by regulation of gene expression
as part of the healing process after acute injury.