ArticleScientific reports2015
Palladin is upregulated in kidney disease and contributes to epithelial cell migration after injury.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Fibroblast-specific palladin drives kidney fibrosis via MRTF-SRF signaling.The Journal of pathology · 2026Article
- Integrated structural model of the palladin-actin complex using XL-MS, docking, NMR, and SAXS.Protein science : a publication of the Protein Society · 2025Article
- The Role of Palladin in Podocytes.Journal of the American Society of Nephrology : JASN · 2018Article
- Article
- Phosphoinositide Binding Inhibits Actin Crosslinking and Polymerization by Palladin.Journal of molecular biology · 2016Article
- High-Throughput Method for Automated Colony and Cell Counting by Digital Image Analysis Based on Edge Detection.PloS one · 2016Article
- Palladin mediates stiffness-induced fibroblast activation in the tumor microenvironment.Biophysical journal · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
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.
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Registered trials
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