ArticleJournal of the American Society of Nephrology : JASN2010
Genetic loci modulate macrophage activity and glomerular damage in experimental glomerulonephritis.
Article in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Animal models for anti-neutrophil cytoplasmic antibody-associated vasculitis: Are current models good enough?Animal models and experimental medicine · 2023Review
- Glomerulonephritis and autoimmune vasculitis are independent of P2RX7 but may depend on alternative inflammasome pathways.The Journal of pathology · 2022Article
- Live Imaging of Monocyte Subsets in Immune Complex-Mediated Glomerulonephritis Reveals Distinct Phenotypes and Effector Functions.Journal of the American Society of Nephrology : JASN · 2020Article
- Spleen tyrosine kinase inhibition is an effective treatment for established vasculitis in a pre-clinical model.Kidney international · 2020Article
- Acute Iron Deprivation Reprograms Human Macrophage Metabolism and Reduces Inflammation In Vivo.Cell reports · 2019Article
- Epoxygenase inactivation exacerbates diet and aging-associated metabolic dysfunction resulting from impaired adipogenesis.Molecular metabolism · 2018Article
- BCAT1 controls metabolic reprogramming in activated human macrophages and is associated with inflammatory diseases.Nature communications · 2017Article
- Identification of Ceruloplasmin as a Gene that Affects Susceptibility to Glomerulonephritis Through Macrophage Function.Genetics · 2017Article
- Identification of a nutrient-sensing transcriptional network in monocytes by using inbred rat models on a cafeteria diet.Disease models & mechanisms · 2016Article
- Macrophage epoxygenase determines a profibrotic transcriptome signature.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Integrating phosphoproteome and transcriptome reveals new determinants of macrophage multinucleation.Molecular & cellular proteomics : MCP · 2015Article
- Kcnn4 is a regulator of macrophage multinucleation in bone homeostasis and inflammatory disease.Cell reports · 2014Article
- Unique regulatory properties of mesangial cells are genetically determined in the rat.PloS one · 2014Article
- Experimental crescentic glomerulonephritis: a new bicongenic rat model.Disease models & mechanisms · 2013Article
- 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
- Genetic susceptibility to experimental autoimmune glomerulonephritis in the Wistar Kyoto rat.The American journal of pathology · 2012Article
- Role of novel rat-specific Fc receptor in macrophage activation associated with crescentic glomerulonephritis.The Journal of biological chemistry · 2012Article
- AP-1 transcription factor JunD confers protection from accelerated nephrotoxic nephritis and control podocyte-specific Vegfa expression.The American journal of pathology · 2011Article
- Characterization of the macrophage transcriptome in glomerulonephritis-susceptible and -resistant rat strains.Genes and immunity · 2011Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
The Wistar Kyoto (WKY) rat is uniquely susceptible to experimentally induced crescentic glomerulonephritis. Two major quantitative trait loci (QTLs) on chromosomes 13 (Crgn1) and 16 (Crgn2) with logarithm of odds >8, as well as five other loci (Crgn3 through 7), largely explain this genetic susceptibility. To understand further the effects of Crgn1 and Crgn2, we generated a double-congenic strain by introgressing these loci from glomerulonephritis-resistant Lewis rats onto the WKY genetic background. Induction of nephrotoxic nephritis in the double-congenic rats (WKY.LCrgn1,2) produced markedly fewer glomerular crescents, reduced macrophage infiltration, and decreased expression of glomerular TNF-alpha and inducible nitric oxide synthase expression compared with control animals. Bone marrow and kidney transplantation studies between parental and WKY.LCrgn1,2 strains, together with in vitro experiments, demonstrated that Crgn1 and Crgn2 contribute exclusively to circulating cell-related glomerular injury by regulating macrophage infiltration and activation. The residual genetic susceptibility to crescentic glomerulonephritis in WKY.LCrgn1,2 rats associated with macrophage activity (especially with enhanced metalloelastase expression) rather than macrophage infiltration. Taken together, these results demonstrate that a genetic influence on macrophage activation, rather than number, determines glomerular damage in immune-mediated glomerulonephritis.
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