ArticleCirculation. Cardiovascular genetics2009
Quantitative trait locus analysis of neointimal formation in an intercross between C57BL/6 and C3H/HeJ apolipoprotein E-deficient mice.
Article in Circulation. Cardiovascular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Article
- Natriuretic Peptide Receptor 2 Locus Contributes to Carotid Remodeling.Journal of the American Heart Association · 2020Article
- Data on genetic linkage of oxidative stress with cardiometabolic traits in an intercross derived from hyperlipidemic mouse strains.Data in brief · 2020Article
- Atherogenesis in the Carotid Artery with and without Interrupted Blood Flow of Two Hyperlipidemic Mouse Strains.Journal of vascular research · 2019Article
- Accelerated atherogenesis in completely ligated common carotid artery of apolipoprotein E-deficient mice.Oncotarget · 2017Article
- Polygenic Control of Carotid Atherosclerosis in a BALB/cJ × SM/J Intercross and a Combined Cross Involving Multiple Mouse Strains.G3 (Bethesda, Md.) · 2017Article
- Mapping and Congenic Dissection of Genetic Loci Contributing to Hyperglycemia and Dyslipidemia in Mice.PloS one · 2016Article
- Background differences in baseline and stimulated MMP levels influence abdominal aortic aneurysm susceptibility.Atherosclerosis · 2015Article
- Genetic linkage of hyperglycemia and dyslipidemia in an intercross between BALB/cJ and SM/J Apoe-deficient mouse strains.BMC genetics · 2015Article
- PET imaging detection of macrophages with a formyl peptide receptor antagonist.Nuclear medicine and biology · 2015Article
- Intima modifier locus 2 controls endothelial cell activation and vascular permeability.Physiological genomics · 2014Article
- Article
- Genetic modification of corneal neovascularization in Dstn (corn1) mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2013Article
- Atherosclerosis susceptibility Loci identified in an extremely atherosclerosis-resistant mouse strain.Journal of the American Heart Association · 2013Article
- Identification of a genetic locus on chromosome 11 that regulates leukocyte infiltration in mouse carotid artery.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- New quantitative trait loci for carotid atherosclerosis identified in an intercross derived from apolipoprotein E-deficient mouse strains.Physiological genomics · 2013Article
- Ribosomal protein L17, RpL17, is an inhibitor of vascular smooth muscle growth and carotid intima formation.Circulation · 2012Article
- Genetic analysis of atherosclerosis and glucose homeostasis in an intercross between C57BL/6 and BALB/cJ apolipoprotein E-deficient mice.Circulation. Cardiovascular genetics · 2012Article
- Genetic modifiers of cardiovascular phenotype caused by elastin haploinsufficiency act by extrinsic noncomplementation.The Journal of biological chemistry · 2011Article
- Hyperglycemia in apolipoprotein E-deficient mouse strains with different atherosclerosis susceptibility.Cardiovascular diabetology · 2011Article
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7 authors.
Funding
Abstract
backgroundInbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit marked differences in neointimal formation after arterial injury when deficient in apolipoprotein E (apoE(-/-)) and fed a Western diet. Quantitative trait locus (QTL) analysis was performed on an intercross between B6.apoE(-/-) and C3H.apoE(-/-) mice to determine genetic factors contributing to the phenotype. METHODS AND
resultsFemale B6.apoE(-/-) mice were crossed with male C3H.apoE(-/-) mice to generate F(1)s, which were intercrossed to generate 204 male F(2) progeny. At 10 weeks of age, F(2)s underwent endothelium denudation injury to the left common carotid artery. Mice were fed a Western diet for 1 week before and 4 weeks after injury and analyzed for neointimal lesion size, plasma lipid and MCP-1 levels. One significant QTL, named Nih1 (61cM, LOD score: 5.02), on chromosome 12 and a suggestive locus on chromosome 13 (35cM, LOD: 2.67) were identified to influence lesion size. One significant QTL on distal chromosome 1 accounted for major variations in plasma non-HDL cholesterol and triglyceride levels. Four suggestive QTLs on chromosomes 1, 2, and 3 were detected for circulating MCP-1 levels. No correlations were observed between neointimal lesion size and plasma lipid levels or between lesion size and plasma MCP-1 levels.
conclusionsNeointimal formation is controlled by genetic factors independent of those affecting plasma lipid levels and circulating MCP-1 levels in the B6 and C3H mouse model.
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