ArticleBMC research notes2014
Death associated protein kinase 2 is expressed in cortical interstitial cells of the mouse kidney.
Article in BMC research notes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 8 citations in OpenAlex.
- Cell profiling of mouse acute kidney injury reveals conserved cellular responses to injury.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Novel Functions of Death-Associated Protein Kinases through Mitogen-Activated Protein Kinase-Related Signals.International journal of molecular sciences · 2018Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDAPK2 is a pro-apoptotic protein kinase that associates with TGFβ receptors. The homolog DAPK1 has been shown to mediate apoptosis in kidney injury. Expression databases indicate that DAPK2 is expressed in the kidney, and in this work we investigate the localization of renal DAPK2 expression and its role in the kidney.
resultsImmunostaining demonstrates DAPK2 expression in interstitial cells of the renal cortex including PDGFRβ-positive pericytes and the CD73-positive erythropoietin-expressing fibroblast population. Tubulointerstitial fibrosis in experimental CKD arises directly from resident interstitial cells, and we therefore evaluated the expression of DAPK2 in the expanded interstitium of mice with kidney disease induced by chronic cisplatin administration. Expanded renal interstitium in these animals was negative for DAPK2 expression, but healthy areas of the kidney in which the tubular interstitium had not expanded expressed DAPK2 at levels similar to the uninjured control. Dapk2 null mice were generated to evaluate if DAPK2 is required for formation of the kidney, or its maintenance in the adult. Kidneys of Dapk2 null mice did not show overt malformations or age-related degeneration, but did show a slight increase in the number of interstitial fibroblasts. Differences were seen between Dapk2 null mice and wild type controls in the response to tubulointerstitial fibrosis caused by chronic cisplatin administration. Although mutant and wild type mice displayed comparable levels of alpha smooth muscle actin, interstitial proliferation and SMAD2 signaling, Dapk2 null mice showed reduced interstitial collagen accumulation.
conclusionsIn the kidney, DAPK2 is strongly and specifically expressed in interstitial cells of the cortex, providing a useful marker for this important cell population. Dapk2 null mice are phenotypically normal under steady state conditions, but display some resistance to extracellular matrix deposition in experimental renal fibrosis indicating that DAPK2 plays a profibrotic role in kidney injury.
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