Palladin is upregulated in kidney disease and contributes to epithelial cell migration after injury

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 funct...

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Bibliographic Details
Published in:Scientific reports 2015-01, Vol.5 (1), p.7695, Article 7695
Main Authors: Chang, Emily H, Gasim, Adil H, Kerber, Michael L, Patel, Julie B, Glaubiger, Samuel A, Falk, Ronald J, Jennette, J Charles, Otey, Carol A
Format: Article
Language:English
Subjects:
Acute Kidney Injury - metabolism
Acute Kidney Injury - pathology
Animals
Cell adhesion & migration
Cell Line
Cell Movement - drug effects
Cell Nucleus - metabolism
Cell proliferation
Cytology
Cytoplasm
Cytoplasm - metabolism
Cytoskeletal Proteins - antagonists & inhibitors
Cytoskeletal Proteins - genetics
Cytoskeletal Proteins - metabolism
Cytoskeleton
Epithelial cells
Epithelial Cells - cytology
Epithelial Cells - metabolism
Gene expression
Humans
Immunohistochemistry
Kidney - pathology
Kidney diseases
Kidney Diseases - metabolism
Kidney Diseases - pathology
Kidney transplantation
Kidneys
Leukocyte migration
Leukocytes (neutrophilic)
Mice
Nuclei
Protein Isoforms - genetics
Protein Isoforms - metabolism
Proximal tubules
RNA Interference
RNA, Small Interfering - metabolism
Rodents
Swine
Transforming Growth Factor beta1 - pharmacology
Transforming growth factor-b1
Up-Regulation - drug effects
Vasculitis
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Summary: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-β1 (TGF-β1) 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-β1 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.
ISSN:2045-2322
2045-2322
DOI:10.1038/srep07695