ArticlePloS one2013
Distinct contributions of TNF receptor 1 and 2 to TNF-induced glomerular inflammation in mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Urinary Complement proteome strongly linked to diabetic kidney disease progression.Nature communications · 2025Article
- Effects triggered by tumor necrosis factor-α in immortalized murine dental pulp and pre-osteoblastic cells.Brazilian oral research · 2025Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- No NLRP3 inflammasome activity in kidney epithelial cells, not even when the NLRP3-A350V Muckle-Wells variant is expressed in podocytes of diabetic mice.Frontiers in immunology · 2023Article
- The Signaling Pathway of TNF Receptors: Linking Animal Models of Renal Disease to Human CKD.International journal of molecular sciences · 2022Review
- Renal microvascular endothelial cell responses in sepsis-induced acute kidney injury.Nature reviews. Nephrology · 2022Review
- Potent anti-inflammatory activity of the lectin-like domain of TNF in joints.Frontiers in immunology · 2022Article
- HO‑1 knockdown upregulates the expression of VCAM‑1 to induce neutrophil recruitment during renal ischemia‑reperfusion injury.International journal of molecular medicine · 2021Article
- YB-1 Interferes with TNFα-TNFR Binding and Modulates Progranulin-Mediated Inhibition of TNFα Signaling.International journal of molecular sciences · 2020Article
- The TNF-derived TIP peptide activates the epithelial sodium channel and ameliorates experimental nephrotoxic serum nephritis.Kidney international · 2019Article
- A new CHO (Chinese hamster ovary)-derived cell line expressing anti-TNFα monoclonal antibody with biosimilar potential.Immunologic research · 2018Article
- Circulating TNF Receptors 1 and 2 Predict Mortality in Patients with End-stage Renal Disease Undergoing Dialysis.Scientific reports · 2017Article
- Is there a role for TNFα blockade in ANCA-associated vasculitis and glomerulonephritis?Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017Review
- Inhibition of ERK1/2 by silymarin in mouse mesangial cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017Article
- TNF/Ang-II synergy is obligate for fibroinflammatory pathology, but not for changes in cardiorenal function.Physiological reports · 2016Article
- The Changing Landscape of Renal Inflammation.Trends in molecular medicine · 2016Review
- Inflammation in diabetic nephropathy: moving toward clinical biomarkers and targets for treatment.Endocrine · 2015Review
- Genetic deletion of TNFR2 augments inflammatory response and blunts satellite-cell-mediated recovery response in a hind limb ischemia model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Etanercept-Induced Anti-Glomerular Basement Membrane Disease.Case reports in nephrology and dialysisArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNF is an important mediator of glomerulonephritis. The two TNF-receptors TNFR1 and TNFR2 contribute differently to glomerular inflammation in vivo, but specific mechanisms of TNFR-mediated inflammatory responses in glomeruli are unknown. We investigated their expression and function in murine kidneys, isolated glomeruli ex vivo, and glomerular cells in vitro. In normal kidney TNFR1 and TNFR2 were preferentially expressed in glomeruli. Expression of both TNFRs and TNF-induced upregulation of TNFR2 mRNA was confirmed in murine glomerular endothelial and mesangial cell lines. In vivo, TNF exposure rapidly induced glomerular accumulation of leukocytes. To examine TNFR-specific inflammatory responses in intrinsic glomerular cells but not infiltrating leukocytes we performed microarray gene expression profiling on intact glomeruli isolated from wildtype and Tnfr-deficient mice following exposure to soluble TNF ex vivo. Most TNF-induced effects were exclusively mediated by TNFR1, including induced glomerular expression of adhesion molecules, chemokines, complement factors and pro-apoptotic molecules. However, TNFR2 contributed to TNFR1-dependent mRNA expression of inflammatory mediators in glomeruli when exposed to low TNF concentrations. Chemokine secretion was absent in TNF-stimulated Tnfr1-deficient glomeruli, but also significantly decreased in glomeruli lacking TNFR2. In vivo, TNF-induced glomerular leukocyte infiltration was abrogated in Tnfr1-deficient mice, whereas Tnfr2-deficiency decreased mononuclear phagocytes infiltrates, but not neutrophils. These data demonstrate that activation of intrinsic glomerular cells by soluble TNF requires TNFR1, whereas TNFR2 is not essential, but augments TNFR1-dependent effects. Previously described TNFR2-dependent glomerular inflammation may therefore require TNFR2 activation by membrane-bound, but not soluble TNF.
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