ArticleGenes and immunity2011
Characterization of the macrophage transcriptome in glomerulonephritis-susceptible and -resistant rat strains.
Article in Genes and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Transcriptomic Analysis of Rat Macrophages.Frontiers in immunology · 2020Article
- Identification of a nutrient-sensing transcriptional network in monocytes by using inbred rat models on a cafeteria diet.Disease models & mechanisms · 2016Article
- 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
- Role of novel rat-specific Fc receptor in macrophage activation associated with crescentic glomerulonephritis.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Crescentic glomerulonephritis (CRGN) is a major cause of rapidly progressive renal failure for which the underlying genetic basis is unknown. Wistar-Kyoto (WKY) rats show marked susceptibility to CRGN, whereas Lewis rats are resistant. Glomerular injury and crescent formation are macrophage dependent and mainly explained by seven quantitative trait loci (Crgn1-7). Here, we used microarray analysis in basal and lipopolysaccharide (LPS)-stimulated macrophages to identify genes that reside on pathways predisposing WKY rats to CRGN. We detected 97 novel positional candidates for the uncharacterized Crgn3-7. We identified 10 additional secondary effector genes with profound differences in expression between the two strains (>5-fold change, <1% false discovery rate) for basal and LPS-stimulated macrophages. Moreover, we identified eight genes with differentially expressed alternatively spliced isoforms, by using an in-depth analysis at the probe level that allowed us to discard false positives owing to polymorphisms between the two rat strains. Pathway analysis identified several common linked pathways, enriched for differentially expressed genes, which affect macrophage activation. In summary, our results identify distinct macrophage transcriptome profiles between two rat strains that differ in susceptibility to glomerulonephritis, provide novel positional candidates for Crgn3-7 and define groups of genes that play a significant role in differential regulation of macrophage activity.
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