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Genes upregulated by homocysteine leading to atherosclerosis

Yi Fu, Xian Wang, Wei Kong
Homocysteine is a sulphur-containing non-proteinogenic amino acid. Hyperhomocysteinaemia (HHcy), the pathogenic elevation of plasma homocysteine as a result of an imbalance of its metabolism, is an independent risk factor for various vascular diseases, such as atherosclerosis, hypertension, vascular calcification and aneurysm. Treatments aimed at lowering plasma homocysteine via dietary supplementation with folic acids and vitamin B are more effective in preventing vascular disease where the population has a normally low folate consumption than in areas with higher dietary folate...
August 24, 2017: British Journal of Pharmacology
Jiang Yi-Deng, Sun Tao, Zhang Hui-Ping, Xiong Jian-Tuan, Cao Jun, Li Gui-Zhong, Wang Shu-Ren
Homocysteine (Hcy) is an important and independent risk factor for arteriosclerosis, and apolipoprotein E (ApoE) is an important gene of anti atherosclerosis, but the characteristics and their key links that are involved in their pathogenic mechanisms are still poorly understood. The objective of the present study was to investigate the effects of Hcy and folate on ApoE as well as the underlying mechanism of ApoE expression induced by Hcy in monocytes. When clinically relevant concentrations of Hcy and folate were added to the cultured monocytes for 4 days, we found that clinically relevant Hcy (100 microM) may increase the levels of total cholesterol (TC), free cholesterol (FC), and cholesteryl ester (CE), and also decrease ApoE mRNA, protein expressions, leading to 34...
October 2007: DNA and Cell Biology
Leonie G Mikael, Jacques Genest, Rima Rozen
Hyperhomocysteinemia, a risk factor for cardiovascular disease, is caused by nutritional or genetic disturbances in homocysteine metabolism. A polymorphism in methylenetetrahydrofolate reductase (MTHFR) is the most common genetic cause of mild hyperhomocysteinemia. To examine mechanisms by which an elevation in plasma homocysteine leads to vascular disease, we first performed microarray analyses in livers of Mthfr-deficient mice and identified differentially expressed genes that are involved in lipid and cholesterol metabolism...
March 3, 2006: Circulation Research
Makiko Maeda, Isamu Yamamoto, Yasushi Fujio, Junichi Azuma
Hyperhomocysteinemia has been reported to be an independent risk factor for atherosclerosis and atherothrombosis. However, the molecular mechanism by which hyperhomocysteinemia can lead to atherosclerosis and atherothrombosis has not been completely described. Vascular endothelial growth factor (VEGF) has been proposed to play an important role in the progression of atherosclerosis. In the present study, we hypothesized that hyperhomocysteinemia might be associated with VEGF expression in atherosclerotic lesions...
September 8, 2003: Biochimica et Biophysica Acta
Chunming Dong, Woohyun Yoon, Pascal J Goldschmidt-Clermont
DNA methylation is a major epigenetic modification of the genome that has the potential to silence gene expression. Recently, the role of epigenetic alteration as a distinct and crucial mechanism to regulate genes governing cell proliferation in atherosclerosis has emerged. Aberrant methylation is related to aging, and, because it affects a large number of CpG islands, age-related methylation may be an important contributor to increased atherosclerosis among older individuals by upregulating atherosclerosis-susceptible genes and downregulating atherosclerosis-protective genes...
August 2002: Journal of Nutrition
H Nonaka, T Tsujino, Y Watari, N Emoto, M Yokoyama
BACKGROUND: Hyperhomocysteinemia is an independent risk factor for atherosclerosis. Homocysteine has been shown to induce endoplasmic reticulum (ER) stress in vascular endothelial cells. ER stress is a condition in which glycoprotein trafficking is disrupted and unfolded proteins accumulate in the ER. ER molecular chaperons, such as GRP78, are induced and an ER resident kinase, PERK, is activated when cells are subjected to ER stress. Conversely, taurine is reported to have antiatherogenic effects by unknown mechanisms...
September 4, 2001: Circulation
R H Böger, K Sydow, J Borlak, T Thum, H Lenzen, B Schubert, D Tsikas, S M Bode-Böger
Asymmetrical dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor. It is formed by protein arginine N-methyltransferases (PRMTs), which utilize S-adenosylmethionine as methyl group donor. ADMA plasma concentration is elevated in hypercholesterolemia, leading to endothelial dysfunction and producing proatherogenic changes of endothelial cell function. Four different isoforms of human PRMTs have been identified. Because the release of ADMA from human endothelial cells is increased in the presence of native or oxidized LDL cholesterol, we investigated the potential involvement of PRMT activity and gene expression in this effect...
July 21, 2000: Circulation Research
G N Welch, G R Upchurch, R S Farivar, A Pigazzi, K Vu, P Brecher, J F Keaney, J Loscalzo
Increased plasma levels of homocysteine are an independent risk factor for atherothrombosis. While the endothelial cytotoxicity of homocysteine has been attributed to oxidative stress associated with the reactivity of the thiol group, the oxidative effect of homocysteine on vascular smooth-muscle cells has not been investigated. Recent evidence suggests that expression of inducible nitric oxide synthase (iNOS), or Nos2 gene product, in vascular smooth-muscle cells may, in part, promote atherosclerosis by increasing local oxidative stress...
January 1998: Proceedings of the Association of American Physicians
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