【摘 要】
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Air pollution has been a major environment-related health threat.Most of the studies on PM2.5 toxicity have verified on the cardiovascular system and endothelial cells.However,researches on PM2.5-indu
【机 构】
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Department of Toxicology and Sanitary Chemistry,School of Public Health,Capital Medical University,B
【出 处】
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首都医科大学公共卫生学院第六届研究生学术论坛
论文部分内容阅读
Air pollution has been a major environment-related health threat.Most of the studies on PM2.5 toxicity have verified on the cardiovascular system and endothelial cells.However,researches on PM2.5-induced myocardial-related toxicity are limited.This study aims to fully understand the toxic effects of PM2.5 on human myocardial cell(AC16)and explore its molecular mechanism based on microarray analysis and bioinformatics analysis.Microarray data analysis manifested that PM2.5-induced toxicity affected expression of 472 genes compared with control group,including 166 up-regulated genes and 306 down-regulated genes in human myocardial (AC16)cells.GO analysis showed that cellular processes such as immune response,cell maturation,embryonic heart tube morphogenesis,cellular response to electrical stimulus,skeletal muscle tissue regeneration and negative regulation of signal transduction were up-regulated,while regulation of transcription(DNA-dependent),rhythmic process,protein destabilization apoptotic process and innate immune response were down-regulated.The pathway analysis indicates that cell signaling pathways such as cytokine-cytokine receptor interaction,NF-κB signaling pathway,chemokine signaling pathway,endocrine and other factor-regulated calcium reabsorption,HTLV-I infection and cell adhesion molecules(CAMs)were up-regulated,while TGF-β signaling pathway was down-regulated.In addition,Signal-net showed that the TUBA4A,ADRBK2,BRIX1,SMC4,EIF5B,PRMT1,ATG4B and NDC80 genes were significantly decreased,while the expression of KRT6B gene was markedly increased compared with control group.All the genes were verified by qRT-PCR This study had provided new bioinformatics evidences in PM2.5-induced myocardial tissue toxicity which is necessary for further cardiovascular system toxicity studies.
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