ArticleAmerican journal of physiology. Renal physiology2019
Global polysome analysis of normal and injured podocytes.
Article in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Functional characterization of podocyte-expressed THSD7A in experimental membranous nephropathy.JCI insight · 2026Article
- Podocyte injury damages podocytes in chimeric organoids.PloS one · 2026Article
- Integrated transcriptomic analysis of LMB2-induced podocyte injury identifies conserved inflammatory and adaptive stress responses.PloS one · 2026Article
- Comprehensive Analysis and Experimental Validation of FOXD2 as a Novel Potential Prognostic Biomarker Associated with Immune Infiltration in Head and Neck Squamous Cell Carcinoma.Current computer-aided drug design · 2025Article
- HDAC6 promotes inflammation in lupus nephritis mice by regulating transcription factors MAFF and KLF5 in renal fibrosis.Renal failure · 2024Article
- LRG1 loss effectively restrains glomerular TGF-β signaling to attenuate diabetic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Implication of transcription factor FOXD2 dysfunction in syndromic congenital anomalies of the kidney and urinary tract (CAKUT).Kidney international · 2024Article
- Forkhead box D subfamily genes in colorectal cancer: potential biomarkers and therapeutic targets.PeerJ · 2024Article
- Early growth response 1 as a podocyte injury marker in human glomerular diseases.Clinical kidney journal · 2024Article
- Dach1 is essential for maintaining normal mature podocytes.PloS one · 2024Article
- Effects of a High-Protein Diet on Kidney Injury under Conditions of Non-CKD or CKD in Mice.International journal of molecular sciences · 2023Article
- C-type lectin-like receptor (CLEC)-2, the ligand of podoplanin, induces morphological changes in podocytes.Scientific reports · 2022Article
- Podocytes are lost from glomeruli before completing apoptosis.American journal of physiology. Renal physiology · 2022Article
- PTPRO knockdown protects against inflammation in hemorrhage shock-induced lung injury involving the NF-κB signaling pathway.Respiratory research · 2022Article
- The Role ofNon-coding RNA · 2022Article
- Article
- Possible kidney-lung cross-talk in COVID-19: in silico modeling of SARS-CoV-2 infection.BMC nephrology · 2022Article
- Profile of Podocyte Translatome During Development of Type 2 and Type 1 Diabetic Nephropathy Using Podocyte-Specific TRAP mRNA RNA-seq.Diabetes · 2021Article
- Indirect podocyte injury manifested in a partial podocytectomy mouse model.American journal of physiology. Renal physiology · 2021Article
- The Inflammatory Process Modulates the Expression and Localization of WT1 in Podocytes Leading to Kidney Damage.In vivo (Athens, Greece)Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Podocyte injury is a key event for progressive renal failure. We have previously established a mouse model of inducible podocyte injury (NEP25) that progressively develops glomerulosclerosis after immunotoxin injection. We performed polysome analysis of intact and injured podocytes utilizing the NEP25 and RiboTag transgenic mice, in which a hemagglutinin tag is attached to ribosomal protein L22 selectively in podocytes. Podocyte-specific polysomes were successfully obtained by immunoprecipitation with an antihemagglutinin antibody from glomerular homogenate and analyzed using a microarray. Compared with glomerular cells, 353 genes were highly expressed and enriched in podocytes; these included important podocyte genes and also heretofore uncharacterized genes, such as Dach1 and Foxd2. Podocyte injury by immunotoxin induced many genes to be upregulated, including inflammation-related genes despite no infiltration of inflammatory cells in the glomeruli. MafF and Egr-1, which structurally have the potential to antagonize MafB and WT1, respectively, were rapidly and markedly increased in injured podocytes before MafB and WT1 were decreased. We demonstrated that Maff and Egr1 knockdown increased the MafB targets Nphs2 and Ptpro and the WT1 targets Ptpro, Nxph3, and Sulf1, respectively. This indicates that upregulated MafF and Egr-1 may promote deterioration of podocytes by antagonizing MafB and WT1. Our systematic microarray study of the heretofore undescribed behavior of podocyte genes may open new insights into the understanding of podocyte pathophysiology.
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