Human coronary artery endothelial cell

Seli E, Pehlivan T, Selam B, Garcia-Velasco JA, Arid A (2002) Estradiol down-regulates MCP-1 expression in human coronary artery endothelial cells. Fertil Steril 77 542-547... 

Li, D., Saldeen, T., Mehta, J.L., 1999, gamma-tocopherol decreases ox-LDL-mediated activation of nuclear factor-kappaB and apoptosis in human coronary artery endothelial cells. Biochem. Biophys. Res. Commun. 259 157-161. 

Tramontane AF, O Leary J, Black AD, Muniyappa R, Cutaia MV, El-Sherif N. Statin decreases endothelial microparticle release from human coronary artery endothelial cells Implication for the Rho-kinase pathway. Biochem Biophys Res Commun 2004 320 34-38. 

Ishida T, Kawashima S, Hirata K, Yokoyama M. Nitric oxide is produced via 5-HT1B and 5-HT2B receptor activation in human coronary artery endothelial cells. Kobe J Med Sci 1998 44 51-63. 

Li, D., Saldeen, T., Romeo, F., et al. 2000. Oxidized LDL upregulates angiotensin II type 1 receptor expression in cultured human coronary artery endothelial cells the potential role of transcription factor NF-kappaB. Circulation 102 1970-1976. 

Li, D., Yang, B., Philips, M.I., and Mehta, J.L. 1999. Proapoptotic effects of ANG II in human coronary artery endothelial cells role of A I i receptor and PKC activation. Am. J. Physiol. 276 H786-H792. 

Zhang LQ, Ma SF, Grigoryev D, Lavoie TL, Xiao HQ, Setterquist R, Li H, Jacobson J, Garcia JG, Ye SQ (2008) Temporal gene expression analysis of human coronary artery endothelial cells treated with Simvastatin. Gene Expr 14 229-239... 

Li D, Mehta JL. Upregulation of endothelial receptor for oxidized LDL (LOX-1) by oxidized LDL and implications in apoptosis of human coronary artery endothelial cells Evidence from use of antisense LOX-1 mRNA and chemical inhihitoTS. Arteriosclerosis, Thrombosis, and Vascular Biology 2000 20 1116-1122. 

Human coronary artery endothelial cells were incubated with epinephrine (10 to 10" M) alone or with the water-soluble analogue of vitamin E (tro-lox) (10 M), the Upid-soluble vitamin E (5 X10" M), or the Pi-adrenergic blocker atenolol (10 M). At 1 and 24 h of incubation with epinephrine, superoxide anion generation increased by 102 and 81 % (Mehta and Li 2001). There was a marked increase in both MnSOD and Cu/ZnSOD mRNA and protein. Both MnSOD and Cu/ZnSOD activities were also increased. Pre-treatment of the cells with trolox and vitamin E decreased superoxide anion generation (P <0.05 vs. epinephrine alone) and blocked the subsequent upregulation of SOD mRNA and protein. Treatment of cells with the P-blocker atenolol also blocked the upregulation of SOD (P <0.05 vs. epinephrine alone). 

Suzuki, Y, Ichiyama, T., Ohsaki, A., et al. 2009. Anti-inflammatory effect of lalpha,25-dihy-droxyvitamin D(3) in human coronary arterial endothelial cells Implication for the treatment of Kawasaki disease. J Steroid Biochem Mol Biol, 113 134—8. 

Human coronary artery endothelial cells. He, W., et al. (2005a)... 

Expression (Human) Tissues Leukocytes, thymus, spleen, liver, ovary Cells PBLs, neutrophils,T-cells, dendritic cells, mast cells, eosinophils, macrophages, leukocytes Tissues spleen, small intestine, placenta, lung smooth muscle, Cells bronchial smooth muscle, CD34+ hemapoietic progenitor cells, monocytes, macrophages, mast cells, eosinophils, neutrophils, PBLs, human umbilical vein endothelial cells Tissues, heart, skeletal muscle, spleen, brain, lymp node, adrenal medulla, lung, human pumonary/ saphenous vein Cells monocytes, macrophages, mast cells, eosinophils, cardiac muscle, coronary artery, PBLs... 

Halichlorine (1) (Fig. 11.1) is an alkaloid which was isolated from the marine sponge H. okadai Kadota (Kuramoto et ah, 1996). This compound was revealed to be a novel alkaloid containing an azaspiro[4.5]decane skeleton clarified by detailed spectroscopic analyses. The absolute stereostructure was confirmed by many synthetic studies (Arimoto et ah, 1998 Clive et ah, 2005 Liu et ah, 2009 Trauner et ah, 1999). Halichlorine was shown to inhibit the induction of vascular cell adhesion molecule-1 (VCAM-1) in cultured human umbilical vein endothelial cells. Drugs that block the inflammatory stimuli-induced expression of VCAM-1 may be useful for treating atherosclerosis, coronary artery diseases, angina, and noncardiovascular inflammatory diseases (Kock et ah, 1995). We introduce here the recent aspects of the biological and physiological activities of halichlorine. 

Endothelial cells located in the vicinity of atherosclerotic lesions, although morphologically intact in the early stages of atherosclerosis, present a number of abnormalities in that they exhibit decreased basal production of NO as well as an impaired responsiveness to endothelium-dependent vasodilators (Drexler et al., 1989). For example, serotonin, which dilates normal human coronary arteries, causes a paradoxical vasoconstriction in... 

Several studies have shown that the extent of coronary artery stenosis due to atherosclerotic plaque formation and expansion into the arterial lumen is not sufficient to explain the incidence of clinical events associated with atherosclerosis [183]. It appears that the generation of clinical events involves plaque mpture, resulting in thrombus formation and arterial occlusion. This mpture is induced by vasomotor disturbances in which oxidized low-density lipoproteins may be involved. Resveratrol is able to regulate vasomotion, which is impaired in atherosclerosis. The key regulators of the vasomotor function are the vasodilator NO and the vasoconstrictor endothelin-1 [167]. A number of in vitro and in vivo studies have shown improved vascular function in response to resveratrol [184, 185]. Resveratrol enhances expression and activity of endothelial nitric oxide synthase [186] and inhibits endothelin-1 secretion and endothelin-1 gene expression in human umbilical vein endothelial cells [187]. Intragastric administration of resveratrol for 12 weeks to hypercholesterolemic rabbits improved the endothelial function, reduced plasma endothelin-1 levels, and induced... 

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