ArticleLaboratory investigation; a journal of technical methods and pathology2011
TNFR2 interposes the proliferative and NF-κB-mediated inflammatory response by podocytes to TNF-α.
Article in Laboratory investigation; a journal of technical methods and pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Pooled it
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- The role of tumor necrosis factor receptor superfamily in cancer: insights into oncogenesis, progression, and therapeutic strategies.NPJ precision oncology · 2025Review
- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- Tsyn-Seq: a T-cell Synapse-Based Antigen Identification Platform.Cancer immunology research · 2024Article
- The role of M1/M2 macrophage polarization in the pathogenesis of obesity-related kidney disease and related pathologies.Frontiers in immunology · 2024Review
- Repurposing drugs for diseases associated with podocyte dysfunction.Kidney international · 2023Review
- Association of Inflammatory Biomarkers With Survival Among Patients With Stage III Colon Cancer.JAMA oncology · 2023Article
- Cell-type-specific molecular characterization of cells from circulation and kidney in IgA nephropathy with nephrotic syndrome.Frontiers in immunology · 2023Article
- Inflammatory biomarkers in staging of chronic kidney disease: elevated TNFR2 levels accompanies renal function decline.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Twist1 in podocytes ameliorates podocyte injury and proteinuria by limiting CCL2-dependent macrophage infiltration.JCI insight · 2021Article
- Childhood HIV-associated nephropathy: 36 years later.Pediatric nephrology (Berlin, Germany) · 2021Review
- TNFα-Induced LDL Cholesterol Accumulation Involve Elevated LDLR Cell Surface Levels and SR-B1 Downregulation in Human Arterial Endothelial Cells.International journal of molecular sciences · 2021Article
- The Impact of β-1,4-Galactosyltransferase V on Microglial Function.Frontiers in cellular neuroscience · 2021Article
- An HIV-Tat inducible mouse model system of childhood HIV-associated nephropathy.Disease models & mechanisms · 2020Article
- Urinary levels of podocyte-derived microparticles are associated with the progression of chronic kidney disease.Annals of translational medicine · 2019Article
- Tumor Necrosis Factor (TNF) Receptor Expression Determines Keratinocyte Fate upon Stimulation with TNF-Like Weak Inducer of Apoptosis.Mediators of inflammation · 2019Article
- Exosomes derived from HIV-1-infected cells promote growth and progression of cancer via HIV TAR RNA.Nature communications · 2018Article
- Podocyte-Specific Induction of Krüppel-Like Factor 15 Restores Differentiation Markers and Attenuates Kidney Injury in Proteinuric Kidney Disease.Journal of the American Society of Nephrology : JASN · 2018Article
- Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis.American journal of physiology. Renal physiology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The development of proliferative podocytopathies has been linked to ligation of tumor necrosis factor receptor 2 (TNFR2) expressed on the renal parenchyma; however, the TNFR2-positive cells within the kidney responsible for podocyte injury are unknown. We detected de novo expression of TNFR2 on podocytes before hyperplastic injury in crescentic glomerulonephritis of mice with nephrotoxic nephritis, and in collapsing glomerulopathy of Tg26(HIV/nl) mice, kd/kd mice, and human beings. We further found that serum levels of soluble TNF-α and TNFR2 correlated significantly with renal injury in Tg26(HIV/nl) mice. Thus, we asked whether ligand binding of TNFR2 on podocytes ex vivo precipitates the characteristic proliferative and pro-inflammatory diseased podocyte phenotypes. Soluble TNF-α activated NF-κB and dose-dependently induced podocyte proliferation, marked by the expression of the podocyte G(1) cyclin and NF-κB target gene, cyclin D1. Microarray gene and chemokine protein expression profiling showed a marked pro-inflammatory NF-κB signature, and activated podocytes secreting CCL2- and CCL5-induced macrophage migration in transwell assays. Neutralization of TNFR2 on podocytes with blocking antibodies abrogated NF-κB activation and the induction of cyclin D1 by TNF-α, and identified TNFR2 as the primary receptor that induced IκBα degradation, the initiating event in NF-κB activation. These results suggest that TNFR2 expressed on podocytes and its canonical NF-κB signaling may directly interpose the compound pathogenic responses by podocytes to TNF-α, in the absence of other TNFR2-positive renal cell types in proliferative podocytopathies.
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