ArticleThe American journal of pathology2011
AP-1 transcription factor JunD confers protection from accelerated nephrotoxic nephritis and control podocyte-specific Vegfa expression.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Transcriptional Regulators YAP and TAZ Have Distinct Abilities to Compensate for One Another in Podocytes.Journal of the American Society of Nephrology : JASN · 2025Article
- Virtual ChIP-seq: predicting transcription factor binding by learning from the transcriptome.Genome biology · 2022Article
- Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury.Science advances · 2020Article
- The family of 14-3-3 proteins and specifically 14-3-3σ are up-regulated during the development of renal pathologies.Journal of cellular and molecular medicine · 2018Article
- The JNK Signaling Pathway in Renal Fibrosis.Frontiers in physiology · 2017Review
- CDK5 functions as a tumor promoter in human colorectal cancer via modulating the ERK5-AP-1 axis.Cell death & disease · 2016Article
- Chronic oxidative stress promotes H2AX protein degradation and enhances chemosensitivity in breast cancer patients.EMBO molecular medicine · 2016Article
- TGF-β-activated kinase 1 is crucial in podocyte differentiation and glomerular capillary formation.Journal of the American Society of Nephrology : JASN · 2014Article
- Combined ChIP-Seq and transcriptome analysis identifies AP-1/JunD as a primary regulator of oxidative stress and IL-1β synthesis in macrophages.BMC genomics · 2013Article
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
Genetic investigation of crescentic glomerulonephritis (Crgn) susceptibility in the Wistar Kyoto rat, a strain uniquely susceptible to nephrotoxic nephritis (NTN), allowed us to positionally clone the activator protein-1 transcription factor Jund as a susceptibility gene associated with Crgn. To study the influence of Jund deficiency (Jund(-/-)) on immune-mediated renal disease, susceptibility to accelerated NTN was examined in Jund(-/-) mice and C57BL/6 wild-type (WT) controls. Jund(-/-) mice showed exacerbated glomerular crescent formation and macrophage infiltration, 10 days after NTN induction. Serum urea levels were also significantly increased in the Jund(-/-) mice compared with the WT controls. There was no evidence of immune response differences between Jund(-/-) and WT animals because the quantitative immunofluorescence for sheep and mouse IgG deposition in glomeruli was similar. Because murine Jund was inactivated by replacement with a bacterial LacZ reporter gene, we then investigated its glomerular expression by IHC and found that the Jund promoter is mainly active in Jund(-/-) podocytes. Furthermore, cultured glomeruli from Jund(-/-) mice showed relatively increased expression of vascular endothelial growth factor A (Vegfa), Cxcr4, and Cxcl12, well-known HIF target genes. Accordingly, small-interfering RNA-mediated JUND knockdown in conditionally immortalized human podocyte cell lines led to increased VEGFA and HIF1A expression. Our findings suggest that deficiency of Jund may cause increased oxidative stress in podocytes, leading to altered VEGFA expression and subsequent glomerular injury in Crgn.
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