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2011 | 58 | 3 |

Tytuł artykułu

Influence of elastin-derived peptides, glucose, LDL and oxLDL on nitric oxide synthase expression in human umbilical artery endothelial cells

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
Endothelial dysfunction plays an important role in the development of atherosclerosis. Elastin-derived peptides (EDP), hyperglycemia, hypercholesterolemia and oxidized LDL have a proven proatherosclerotic potential. Nitric oxide generated by endothelial nitric oxide synthase (eNOS; EC 1.14.13.39) is an important vasorelaxant. Here we studied the influence of those proatherosclerotic factors on eNOS gene and protein expression in artery-derived endothelial cells. Human umbilical artery endothelial cells (HUAEC) were incubated with or without: glucose (270 mg/dl), LDL (200 mg/dl), oxidized LDL (oxLDL 25 mg/dl) or κ-elastin (0.5 and 2.5 µg/ml). Gene expression was assessed by real time RT-PCR, whilst the eNOS protein by ELISA. In cells incubated with 2.5 µg/ml of κ-elastin, a 31 % increase of eNOS mRNA expression was observed, but the protein level remained unchanged. OxLDL, LDL and glucose decreased the eNOS protein level by 74 %, 37 % and 29 %, respectively. OxLDL decreased eNOS mRNA by 42 %. LDL non-significantly decreased eNOS mRNA expression. An elevated glucose level did not affect the eNOS mRNA expression. Hyperglycemia and an elevated level of LDL, particularly oxLDL, decreased the level of eNOS protein in endothelial cells. As κ-elastin did not decrease the expression of eNOS gene in HUAEC, the proatherogenic properties of elastin-derived peptides are unlikely to be due to their influence on eNOS.

Wydawca

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Rocznik

Tom

58

Numer

3

Opis fizyczny

p.375-379,fig.,ref.

Twórcy

autor
  • Department of Biochemistry, Medical University of Silesia, Katowice, Poland
autor
autor
autor
autor

Bibliografia

  • Braam B, Verhaar MC (2007) Understanding eNOS for pharmacological modulation of endothelial function: a translational view. Curr Pharm Des 13: 1727-1740. 
  • Cai H, Harrison DG (2000) Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress. Circ Res 87: 840-844. 
  • Cosentino F, Hishikawa K, Katusic ZS, Luscher TF (1997) High glucose increases nitric oxide synthase expression and superoxide anion generation in human aortic endothelial cells. Circulation 96: 25-28. 
  • Dötsch J, Hogen N, Nyúl Z, Hänze J, Knerr I, Kirschbaum M, Rascher W (2001) Increase of endothelial nitric oxide synthase and endothelin-1 mRNA expression in human placenta during gestation. Eur J Obstet Gynecol Reprod Biol 97: 163-167. 
  • Faury G, Ristori MT, Verdetti J, Jacob MP, Robert L (1995) Effect of elastin peptides on vascular tone. J Vasc Res 32: 112-119. 
  • Faury G, Garnier S, Weiss AS, Wallach J, Fülöp T Jr, Jacob MP, Mecham RP, Robert L, Verdetti J (1998) Action of tropoelastin and synthetic elastin sequences on vascular tone and on free Ca2+ level in human vascular endothelial cells. Circ Res 82: 328-336. 
  • Fulop T Jr, Wei SM, Robert L, Jacob MP (1990) Determination of elastin peptides in normal and arteriosclerotic human sera by ELISA. Clin Physiol Biochem 8: 273-282. 
  • Fulop T Jr, Larbi A, Fortun A, Robert L, Khalil A (2005) Elastin peptides induced oxidation of LDL by phagocytic cells. Pathol Biol (Paris) 53: 416-423. 
  • Galle J, Wanner C (1998) Oxidized LDL and Lp(a). Preparation, modification, and analysis. Methods Mol Biol 108: 119-130. 
  • Garland J (2002) Isolation of LDL (low density lipoprotein) from human plasma. www.protocol-online.org 2002; access: 15 May 2010 http://www.protocol-online.org/cgi-bin/prot/view_cache.cgi?ID=2520
  • Gmiński J, Dróżdż M (1991) Succinyl trialanine p-nitroanilide hydrolytic activities in plasma and the aorta of rabbits experimentally immunized with soluble elastin. Exp Pathol 43: 37-40. 
  • Gmiński J, Dróżdż M, Ulfig-Maślanka R, Najda J (1991) Evaluation of elastin metabolism in children from families with high risk of atherosclerosis. Atherosclerosis 91: 185-189. 
  • Hornebeck W, Robert L (1977) Elastase-like enzymes in aortas and human brest carcinomas: quantitative variations with age and pathology. Adv Exp Med Biol 79: 145-156. 
  • Jiménez A, Arriero MM, López-Blaya A, González-Fernandez F, García R, Fortes J, Millás I, Velasco S, Sánchez De Miguel L, Rico L, Farré J, Casado S, López-Farré A (2001) Regulation of endothelial nitric oxide synthase expression in the vascular wall and in mononuclear cells from hypercholesterolemic rabbits. Circulation 104: 1822-1830. 
  • Liao JK, Shin WS, Lee WY, Clark SL (1995) Oxidized low-density lipoprotein decreases the expression of endothelial nitric oxide synthase. J Biol Chem 270: 319-324. 
  • Liaudet L, Vassalli G, Pacher P (2009) Role of peroxynitrite in the redox regulation of cell signal transduction pathways. Front Biosci 14: 4809-4814. 
  • Ogut O, Brozovich FV (2008) The potential role of MLC phosphatase and MAPK signalling in the pathogenesis of vascular dysfunction in heart failure. J Cell Mol Med 12: 2158-2164. 
  • Pritchard KA, Ackerman AW, Ou J, Curtis M, Smalley DM, Fontana JT, Stemerman MB, Sessa WC (2002) Native low-density lipoprotein induces endothelial nitric oxide synthase dysfunction: role of heat shock protein 90 and caveolin-1. Free Radic Biol Med 33: 52-62. 
  • Robert L, Labat-Robert J, Robert AM (2010) Genetic, epigenetic and posttranslational mechanisms of aging. Biogerontology DOI: 10.1007/s10522-010-9262-y. 
  • Ross R (1999) Atherosclerosis - an inflammatory disease. N Engl J Med 340: 115-126. 
  • Srinivasan S, Hatley ME, Bolick DT, Palmer LA, Edelstein D, Brownlee M, Hedrick CC (2004) Hyperglycaemia-induced superoxide production decreases eNOS expression via AP-1 activation in aortic endothelial cells. Diabetologia 47: 1727-1734. 
  • Stone NJ, Bilek S, Rosenbaum S (2005) Recent National Cholesterol Education Program Adult Treatment Panel III update: adjustments and options. Am J Cardiol 96: 53E-59E. 

Typ dokumentu

Bibliografia

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Identyfikator YADDA

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