Prenatal arsenic exposure alters gene expression in the adult liver to a proinflammatory state contributing to accelerated atherosclerosis

The mechanisms by which environmental toxicants alter developmental processes predisposing individuals to adult onset chronic disease are not well-understood. Transplacental arsenic exposure promotes atherogenesis in apolipoprotein E-knockout (ApoE(-/-)) mice. Because the liver plays a central role...

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Veröffentlicht in:	PloS one 2012-06, Vol.7 (6), p.e38713
Hauptverfasser:	States, J Christopher, Singh, Amar V, Knudsen, Thomas B, Rouchka, Eric C, Ngalame, Ntube O, Arteel, Gavin E, Piao, Yulan, Ko, Minoru S H
Format:	Artikel
Sprache:	eng
Schlagworte:	Acids Animals Annotations Antigen presentation Antigen processing Antigens Apolipoprotein E Apolipoproteins Apoptosis Arsenic Arsenic - toxicity Arteriosclerosis Arthritis Atherogenesis Atherosclerosis Atherosclerosis - etiology Binding sites Bioinformatics Biology Blotting, Western Cancer Cardiovascular diseases Cascades Chronic diseases Chronic illnesses Clustering Coagulation Data analysis Diabetes Diabetes mellitus DNA microarrays Drinking water Endoplasmic reticulum Environmental toxicology Exposure Female Fetuses Gene expression Gene Expression Regulation - drug effects Genes Genetics Genomes Genomics Gluconeogenesis Glycolysis Health risk assessment Heat shock Heat shock proteins Hepatocyte nuclear factor 4 Hsp70 protein Hybridization Immunoglobulin M Inflammation Laboratories Liver Liver - drug effects Liver - metabolism Liver diseases Medicine Messenger RNA Metabolic disorders Metabolic syndrome Mice Mice, Knockout MicroRNA MicroRNAs - genetics miRNA Models, Animal Oxidative stress Pathways Pharmacology Pregnancy Pregnant women Prenatal experience Prenatal Exposure Delayed Effects Protein transport Rheumatoid arthritis Rheumatoid factor Ribonucleic acid RNA RNA, Messenger - genetics Studies Toxicants Toxicology Tumors Type 2 diabetes
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