ArticleAlcoholism, clinical and experimental research2013
Genetic resistance to liver fibrosis on A/J mouse chromosome 17.
Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 10 citations in OpenAlex.
- Differential sensitivity of inbred mouse strains to ovarian damage in response to low-dose total body irradiation†.Biology of reproduction · 2020Article
- Genome Sequencing of Chromosome 1 Substitution Lines Derived from Chinese Wild Mice Revealed a Unique Resource for Genetic Studies of Complex Traits.G3 (Bethesda, Md.) · 2016Article
- Linking Pathogenic Mechanisms of Alcoholic Liver Disease With Clinical Phenotypes.Gastroenterology · 2016Review
- Contrasting genetic architectures in different mouse reference populations used for studying complex traits.Genome research · 2015Review
- Constitutive Activation of the Nlrc4 Inflammasome Prevents Hepatic Fibrosis and Promotes Hepatic Regeneration after Partial Hepatectomy.Mediators of inflammation · 2015Article
- Inflammatory PAF Receptor Signaling Initiates Hedgehog Signaling and Kidney Fibrogenesis During Ethanol Consumption.PloS one · 2015Article
- Genetic determinants of atherosclerosis, obesity, and energy balance in consomic mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Article
- Carotid body denervation prevents fasting hyperglycemia during chronic intermittent hypoxia.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- The role of mouse strain differences in the susceptibility to fibrosis: a systematic review.Fibrogenesis & tissue repair · 2013Article
- Alcohol-induced liver injury is modulated by Nlrp3 and Nlrc4 inflammasomes in mice.Mediators of inflammation · 2013Article
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15 authors at 5 institutions in 1 country.
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Abstract
backgroundBecause the histological and biochemical progression of liver disease is similar in alcoholic steatohepatitis (ASH) and nonalcoholic steatohepatitis (NASH), we hypothesized that the genetic susceptibility to these liver diseases would be similar. To identify potential candidate genes that regulate the development of liver fibrosis, we studied a chromosome substitution strain (CSS-17) that contains chromosome 17 from the A/J inbred strain substituted for the corresponding chromosome on the C57BL/6J (B6) genetic background. Previously, we identified quantitative trait loci (QTLs) in CSS-17, namely obesity-resistant QTL 13 and QTL 15 (Obrq13 and Obrq15, respectively), that were associated with protection from diet-induced obesity and hepatic steatosis on a high-fat diet.
methodsTo test whether these or other CSS-17 QTLs conferred resistance to alcohol-induced liver injury and fibrosis, B6, A/J, CSS-17, and congenics 17C-1 and 17C-6 were either fed Lieber-DeCarli ethanol (EtOH)-containing diet or had carbon tetrachloride (CCl4 ) administered chronically.
resultsThe congenic strain carrying Obrq15 showed resistance from alcohol-induced liver injury and liver fibrosis, whereas Obrq13 conferred susceptibility to liver fibrosis. From published deep sequencing data for chromosome 17 in the B6 and A/J strains, we identified candidate genes in Obrq13 and Obrq15 that contained single-nucleotide polymorphisms (SNPs) in the promoter region or within the gene itself. NADPH oxidase organizer 1 (Noxo1) and NLR family, CARD domain containing 4 (Nlrc4) showed altered hepatic gene expression in strains with the A/J allele at the end of the EtOH diet study and after CCl4 treatment.
conclusionsAspects of the genetics for the progression of ASH are unique compared to NASH, suggesting that the molecular mechanisms for the progression of disease are at least partially distinct. Using these CSSs, we identified 2 candidate genes, Noxo1 and Nlrc4, which modulate genetic susceptibility in ASH.
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