ArticleAtherosclerosis2010
Differential expression of genes in the calcium-signaling pathway underlies lesion development in the LDb mouse model of atherosclerosis.
Article in Atherosclerosis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- DNA methylation profiling reveals novel pathway implicated in cardiovascular diseases of diabetes.Frontiers in endocrinology · 2023Article
- Favine/CCDC3 deficiency accelerated atherosclerosis and thrombus formation is associated with decreased MEF2C-KLF2 pathway.iScience · 2022Article
- A Critical Role of PCSK9 in Mediating IL-17-Producing T Cell Responses in Hyperlipidemia.Immune network · 2019Article
- PCSK9 deficiency reduces atherosclerosis, apolipoprotein B secretion, and endothelial dysfunction.Journal of lipid research · 2018Article
- Effects of chlorogenic acid on intracellular calcium regulation in lysophosphatidylcholine-treated endothelial cells.BMB reports · 2017Article
- Comparative transcriptomic analysis of mice liver treated with different AMPK activators in a mice model of atherosclerosis.Oncotarget · 2017Article
- Detection and Characterization of the Effect of AB-FUBINACA and Its Metabolites in a Rat Model.Journal of cellular biochemistry · 2016Article
- Identification of novel genes and pathways in carotid atheroma using integrated bioinformatic methods.Scientific reports · 2016Article
- Foamy monocytes form early and contribute to nascent atherosclerosis in mice with hypercholesterolemia.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Fortilin reduces apoptosis in macrophages and promotes atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2013Article
- Long-term Expression of Apolipoprotein B mRNA-specific Hammerhead Ribozyme via scAAV8.2 Vector Inhibits Atherosclerosis in Mice.Molecular therapy. Nucleic acids · 2013Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveAtherosclerosis is influenced by the interaction of environmental and genetic susceptibility risk factors. We used global microarray expression profiling to investigate differentially regulated genes in aorta during development of atherosclerosis in a susceptible genetically modified mouse model in response to the interaction between risk factors including hyperlipidemic genotype, shear stress, diet, and age. METHODS AND
resultsIn this study we investigated transcriptional changes in lesion-prone and lesion-resistant regions of aortas in genetically modified mice lacking both genes of the LDL receptor and the apolipoprotein B mRNA editing enzyme (LDb; Ldlr(-/-)Apobec1(-/-)). Risk factors including hyperlipidemic genotype (LDb vs. C57BL/6 wildtype), shear stress (lesion-prone vs. lesion resistant aortic regions), diet (chow vs. Western high-fat), and age (2- vs. 8-months) were studied. We hybridized aortic RNA samples with microarray chips containing probes for 45,000 mouse genes and expressed sequence tags (ESTs). Overall, the differentially expressed genes were components of 20 metabolic and physiological pathways. Notably, calcium signaling is the major pathway identified with differential regulation of 30 genes within this pathway. We also found differential expression of calcium-signaling genes in cultured primary endothelial cells from lesion-prone and lesion-resistant arterial regions (LDb mice vs. C57BL/6 controls), providing further support for involvement of calcium signaling in the pathogenesis of atherosclerosis. Moreover, we demonstrated protein expression of genes in the calcium-signaling pathway using Western blot analysis and immunofluorescence.
conclusionsOur results suggest that calcium signaling may play an important role in regulation of genes expressed in aorta during development of atherosclerosis. Calcium signaling may act via mechanistic responses to genetic, mechanical, and environmental insults that trigger an imbalance of intracellular calcium homeostasis, resulting in altered biological processes leading to lesion development.
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