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Genes upregulated by hyperhomocysteinemia

Peng Li, Ya-Ling Yin, Tao Guo, Xue-Ying Sun, Hui Ma, Mo-Li Zhu, Fan-Rong Zhao, Ping Xu, Yuan Chen, Guang-Rui Wan, Fan Jiang, Qi-Sheng Peng, Chao Liu, Li-Ying Liu, Shuang-Xi Wang
BACKGROUND: -GTP cyclohydrolase 1 (GCH1) deficiency is critical for endothelial nitric oxide synthase (eNOS) uncoupling in endothelial dysfunction. MicroRNAs (miR) are a class of regulatory RNAs that negatively regulate gene expression. We investigated whether statins prevent endothelial dysfunction via miR-dependent GCH1 upregulation. METHODS: -Endothelial function was assessed by measuring acetylcholine- induced vasorelaxation in the organ chamber. MiR-133a expression was assessed by RT-qPCR and fluorescence in situ hybridization...
October 20, 2016: Circulation
Luis G Rabaneda, Noelia Geribaldi-Doldán, Maribel Murillo-Carretero, Manuel Carrasco, José M Martínez-Salas, Cristina Verástegui, Carmen Castro
Hyperhomocysteinemia reduces neurogenesis in the adult mouse brain. Homocysteine (Hcy) inhibits postnatal neural progenitor cell (NPC) proliferation by specifically impairing the fibroblast growth factor receptor (FGFR)-Erk1/2-cyclin E signaling pathway. We demonstrate herein that the inhibition of FGFR-dependent NPC proliferation induced by Hcy is mediated by its capacity to alter the cellular methylation potential. Our results show that this alteration modified the expression pattern and activity of Sprouty2 (Spry2), a negative regulator of the above mentioned pathway...
September 26, 2016: Biochimica et Biophysica Acta
Amany Tawfik, Sylvia B Smith
Hyperhomocysteinemia is implicated in retinal neurovascular diseases including arterial occlusive disease, venous occlusive disease and pseudoexfoliation glaucoma. The mechanism for these diseases is not known. Here we used hyperhomocysteinemic mice lacking the gene encoding cystathionine-beta-synthase (cbs (-/-)) to examine whether ER stress could be a mechanism for the retinal neurovasculopathy reported in these mice. Retinas of cbs (+/+) and cbs (-/-) mice (age: 3-5 wks) were used to investigate the expression of ER stress genes (BiP/GRP78, Perk, Atf6, Atf4, Ire1α, Chop) and the proteins they encode...
June 16, 2014: Austin Journal of Clinical Ophthalmology
Min Fang, Jing Wang, Han Yan, Yan-Xin Zhao, Xue-Yuan Liu
High levels of homocysteine, caused by abnormal methionine metabolism, can induce degeneration of mouse hippocampal neurons. iTRAQ™ technology has been widely used in the field of proteomics research and through employing this technology, the present study identified that hyperhomocysteinemia induced the downregulation of 52 proteins and upregulation of 44 proteins in the mouse hippocampus. Through gene ontology and pathway analysis, the upregulation of components of the cytoskeleton, actin, regulators of focal adhesion, calcium signaling pathways, tight junctions, ErbB and gonadotrophin‑releasing hormone signaling, leukocyte, transendothelial migration, propanoate and pyruvate metabolism, valine, leucine and isoleucine biosynthesis, synthesis and degradation of ketone bodies and benzoate degradation via CoA ligation pathway, was identified...
November 2014: Molecular Medicine Reports
Xin-xia Chang, Hong-mei Yan, Qiong Xu, Ming-feng Xia, Hua Bian, Teng-fang Zhu, Xin Gao
BACKGROUND: The study was undertaken to examine the effects of berberine (BBR) on serum homocysteine, lipids and the aortic lesion in Sprague-Dawley (SD) rats fed with a long-term high-fat diet (HFD). METHODS: Healthy male SD rats weighing 190-210 g received randomly standard diet or a high-fat diet for 24 weeks. After 8 weeks of feeding, rats fed with HFD were randomized to receive berberine (200 mg · kg-1· day-1) or vehicle by gavage for 16 weeks. After overnight fasting, all rats were sacrificed and total blood samples were also collected for determinant of fasting serum homocysteine (Hcy), total cholesterol (TC) and low density lipoprotein cholesterol (LDL-c) levels...
2012: Lipids in Health and Disease
Utpal Sen, Pushpakumar B Sathnur, Sourav Kundu, Srikanth Givvimani, Denise M Coley, Paras K Mishra, Natia Qipshidze, Neetu Tyagi, Naira Metreveli, Suresh C Tyagi
Hydrogen sulfide (H(2)S) has recently been identified as a regulator of various physiological events, including vasodilation, angiogenesis, antiapoptotic, and cellular signaling. Endogenously, H(2)S is produced as a metabolite of homocysteine (Hcy) by cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST). Although Hcy is recognized as vascular risk factor at an elevated level [hyperhomocysteinemia (HHcy)] and contributes to vascular injury leading to renovascular dysfunction, the exact mechanism is unclear...
July 1, 2012: American Journal of Physiology. Cell Physiology
Donghong Zhang, Xina Xie, Yequn Chen, Bruce D Hammock, Wei Kong, Yi Zhu
RATIONALE: Hyperhomocysteinemia is a risk factor of atherogenesis. Soluble epoxide hydrolase (sEH) is a major enzyme that hydrolyzes epoxyeicosatrienoic acids and attenuates their cardiovascular protective effects. Whether homocysteine (Hcy) regulates sEH and the underlying mechanism remains elusive. OBJECTIVE: To elucidate the mechanism by which Hcy regulates sEH expression and endothelial activation in vitro and in vivo. METHODS AND RESULTS: Hcy treatment in cultured human endothelial cells dose-dependently and time-dependently upregulated sEH mRNA and protein...
March 16, 2012: Circulation Research
Chun Zhang, Fan Yi, Min Xia, Krishna M Boini, Qing Zhu, Laura A Laperle, Justine M Abais, Christopher A Brimson, Pin-Lan Li
This study investigated the role of NMDA receptor in hyperhomocyteinemia (hHcys)-induced NADPH oxidase (Nox) activation and glomerulosclerosis. Sprague-Dawley rats were fed a folate-free (FF) diet to produce hHcys, and a NMDA receptor antagonist, MK-801, was administrated. Rats fed the FF diet exhibited significantly increased plasma homocysteine levels, upregulated NMDA receptor expression, enhanced Nox activity and Nox-dependent O(2)(.-) production in the glomeruli, which were accompanied by remarkable glomerulosclerosis...
October 1, 2010: Antioxidants & Redox Signaling
Xue Yu, Youguang Huang, Qiang Hu, Lanqing Ma
Homocysteine is an intermediate in the sulfur amino acid metabolism. Recent studies suggested that there might be links between hyperhomocysteinemia and insulin resistance. In the present study, we investigated the effect of homocysteine on glucose metabolism. We demonstrated that the levels of insulin were significantly higher in mice with hyperhomocysteinemia than those in the normal mice after administration of glucose. The effect of insulin on glucose output was significantly blocked in the homocysteine-treated hepatocytes...
December 2009: Acta Biochimica et Biophysica Sinica
Yin Li, Changtao Jiang, Guoheng Xu, Nanping Wang, Yi Zhu, Chaoshu Tang, Xian Wang
OBJECTIVE: Homocysteine (Hcy) is epidemiologically related to insulin resistance, which has been speculated to be a low-grade systemic inflammatory condition. Resistin acts as a critical mediator of insulin resistance associated with inflammatory conditions. We aimed to determine whether Hcy can induce insulin resistance by directly regulating the expression and secretion of resistin from adipose tissue. RESEARCH DESIGN AND METHODS: The effect of Hcy on the expression and secretion of resistin and insulin resistance was investigated using primary rat adipocytes and mice with hyperhomocysteinemia (HHcy)...
April 2008: Diabetes
Utpal Sen, Neetu Tyagi, Munish Kumar, Karni S Moshal, Walter E Rodriguez, Suresh C Tyagi
Although elevated levels of homocysteine (Hcy) known as hyperhomocysteinemia (HHcy) are associated with increased inflammation and vascular remodeling, the mechanism of Hcy-mediated inflammation and vascular remodeling is unclear. The matrix metalloproteinases (MMPs) and adhesion molecules play an important role in vascular remodeling. We hypothesized that HHcy induces inflammation by increasing adhesion molecules and matrix protein expression. Endothelial cells were supplemented with high methionine, and Hcy accumulation was measured by HPLC...
December 2007: American Journal of Physiology. Cell Physiology
Julien Hamelet, Karine Demuth, Jean-Louis Paul, Jean-Maurice Delabar, Nathalie Janel
BACKGROUND/AIMS: Cystathionine beta synthase (CBS) deficiency leads to severe hyperhomocysteinemia, which confers diverse clinical manifestations, notably fatty liver. Recently, abnormal lipid metabolism has been demonstrated in CBS-deficient mice, a murine model of severe hyperhomocysteinemia. To gain further insights into effects of CBS deficiency on hepatic cholesterol metabolism, the expression of hepatic genes involved in biosynthesis, uptake and efflux was determined in CBS-deficient mice...
January 2007: Journal of Hepatology
Liselotte S Ebbesen, Sanne H Olesen, Mogens Kruhøffer, Jørgen Ingerslev, Torben F Ørntoft
Hyperhomocysteinemia (HH) is an independent risk factor for thrombosis although the precise pathogenesis is still unresolved. Previous studies have demonstrated that HH changes whole blood coagulation by increasing the velocity, increasing the firmness of the formed clot, and by prolonging the initiation phase of the coagulation. With the aim of elucidating the genetic pathogenesis which might be responsible for the changes in whole blood coagulation, we applied oligo-array technology to RNA from buffycoat-cells comparing animals suffering from hyperhomocysteinemia (42 micromol/l) with controls (6 micromol/l)...
June 2006: Blood Coagulation & Fibrinolysis: An International Journal in Haemostasis and Thrombosis
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
Toshimitsu Suhara, Keisuke Fukuo, Osamu Yasuda, Maki Tsubakimoto, Yukihiro Takemura, Hidenobu Kawamoto, Toyohiko Yokoi, Masaki Mogi, Taeko Kaimoto, Toshio Ogihara
Hyperhomocysteinemia is an independent risk factor for the development of atherosclerosis. However, the underlying mechanism of endothelial cell injury in hyperhomocysteinemia has not been elucidated. In this study, we examined the effect of homocysteine (Hcy) on Fas-mediated apoptosis in endothelial cells. Hcy-induced upregulation of Fas in endothelial cells (ECs) in a dose-dependent manner. At the same time, Hcy increased intracellular peroxide in ECs. Hcy-induced Fas expression was inhibited by the treatment with catalase...
June 2004: Hypertension
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
E R García-Tevijano, C Berasain, J A Rodríguez, F J Corrales, R Arias, A Martín-Duce, J Caballería, J M Mato, M A Avila
Numerous clinical and epidemiological studies have identified elevated homocysteine levels in plasma as a risk factor for atherosclerotic vascular disease and thromboembolism. Hyperhomocysteinemia may develop as a consequence of defects in homocysteine-metabolizing genes; nutritional conditions leading to vitamin B(6), B(12), or folate deficiencies; or chronic alcohol consumption. Homocysteine is an intermediate in methionine metabolism, which takes place mainly in the liver. Impaired liver function leads to altered methionine and homocysteine metabolism; however, the molecular basis for such alterations is not completely understood...
November 2001: Hypertension
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 Poddar, N Sivasubramanian, P M DiBello, K Robinson, D W Jacobsen
BACKGROUND: Proinflammatory cytokines play key roles in atherogenesis and disease progression. Because hyperhomocysteinemia is an independent risk factor for cardiovascular disease, we hypothesized that homocysteine could be atherogenic by altering the expression of specific cytokines in vascular endothelial cells. METHODS AND RESULTS: Northern blot and RNase protection assays showed that DL-homocysteine induced mRNA expression of the proinflammatory cytokines monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) in cultured human aortic endothelial cells (HAECs)...
June 5, 2001: Circulation
K Kokame, H Kato, T Miyata
Hyperhomocysteinemia is known to be a risk factor for arteriosclerosis and thrombosis. To elucidate the mechanisms by which homocysteine may promote vascular diseases, we have applied a modified nonradioactive differential display analysis that evaluates changes in gene expression induced by homocysteine treatment of cultured human umbilical vein endothelial cells (HUVECs). We identified six upregulated and one downregulated gene. One upregulated gene was GRP78/BiP, an endoplasmic reticulum (ER)-resident molecular chaperone, suggesting that unfolded proteins would accumulate in the ER because of redox potential changes caused by homocysteine...
December 1998: Methods: a Companion to Methods in Enzymology
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