ArticleCell death & disease2016
GADD45B mediates podocyte injury in zebrafish by activating the ROS-GADD45B-p38 pathway.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
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- Mitochondrial Oxidative Stress and Cell Death in Podocytopathies.Biomolecules · 2022Review
- Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022Review
- FTO-mediated demethylation of GADD45B promotes myogenesis through the activation of p38 MAPK pathway.Molecular therapy. Nucleic acids · 2021Article
- Evaluation of endogenous miRNA reference genes across different zebrafish strains, developmental stages and kidney disease models.Scientific reports · 2021Article
- Super-Enhancer-Associated Transcription Factors Maintain Transcriptional Regulation in Mature Podocytes.Journal of the American Society of Nephrology : JASN · 2021Article
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Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
GADD45 gene has been implicated in cell cycle arrest, cell survival or apoptosis in a cell type specific and context-dependent manner. Members of GADD45 gene family have been found differentially expressed in several podocyte injury models, but their roles in podocytes are unclear. Using an in vivo zebrafish model of inducible podocyte injury that we have previously established, we found that zebrafish orthologs of gadd45b were induced upon the induction of podocyte injury. Podocyte-specific overexpression of zebrafish gadd45b exacerbated edema, proteinuria and foot-process effacement, whereas knockdown of gadd45b by morpholino-oligos in zebrafish larvae ameliorated podocyte injury. We then explored the role of GADD45B induction in podocyte injury using in vitro podocyte culture. We confirmed that GADD45B was significantly upregulated during the early phase of podocyte injury in cultured human podocytes and that podocyte apoptosis induced by TGF-β and puromycin aminonucleoside (PAN) was aggravated by GADD45B overexpression but ameliorated by shRNA-mediated GADD45B knockdown. We also showed that ROS inhibitor NAC suppressed PAN-induced GADD45B expression and subsequent activation of p38 MAPK pathway in podocytes and that inhibition of GADD45B diminished PAN-induced p38 MAPK activation. Taken together, our findings demonstrated that GADD45B has an important role in podocyte injury and may be a therapeutic target for the management of podocyte injury in glomerular diseases.
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