Modulation of human monocyte CD36 by type 2 diabetes mellitus and other atherosclerotic risk factors

被引:13
作者
Bernal-Lopez, Rosa M. [2 ]
Llorente-Cortes, Vicenta [3 ]
Lopez-Carmona, Dolores [4 ]
Mayas, Dolores M. [2 ]
Gomez-Huelgas, Ricardo [4 ]
Tinahones, Francisco J. [1 ,2 ]
Badimon, Lina [2 ,3 ]
机构
[1] Hosp Virgen de la Victoria, Serv Endocrinol, Biomed Res Lab, Dept Endocrinol, Malaga 29010, Spain
[2] Inst Salud Carlos III, Ciber Fisiopatol Obesidad Nutr CB06 003, Madrid, Spain
[3] Hosp Santa Creu & Sant Pau, CSIC ICCC, Cardiovasc Res Ctr, Barcelona, Spain
[4] Hosp Carlos Haya, Dept Internal Med, Malaga, Spain
关键词
Atherothrombosis; CD36; diabetes; Hb1Ac; monocytes; SCAVENGER RECEPTOR CD36; EXPRESSION; INHIBITION; PROTEIN; CELLS; LDL;
D O I
10.1111/j.1365-2362.2011.02475.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background The pathophysiological role of CD36 in atherosclerosis seems to be largely dependent on its proinflammatory function and ability to take up oxidized low-density lipoprotein. Controversy exists concerning the potential beneficial/harmful effects of vascular CD36 inhibition in atherosclerosis. However, as atherosclerosis in murine models does not result in clinical end points such as plaque rupture and thrombotic ischaemia, typical of human disease, clinical studies are required to understand the functional role of CD36 in human atherosclerosis. Materials and methods Our aim was to investigate whether CD36 expression in monocytes is modulated by the presence of an increasing number of atherosclerotic risk factors, and specifically by hyperglycaemia because of diabetes mellitus. The study included 33 patients with advanced atherosclerosis and eight healthy blood donors, as controls. The patients were classified according to the presence of atherosclerotic risk factors. Diabetes mellitus was classified as either well-controlled or poorly controlled. Monocytes were exposed in vitro to low (5.5 mM) or high glucose (26 mM) concentrations for increasing times. Results Our results demonstrated that protein levels of glycated CD36 were significantly higher in patients with 3-4 atherosclerotic risk factors than in those with 0-2 atherosclerotic risk factors or in subjects with no atherosclerotic symptoms (P = 0.04, in both cases). However, when we analysed just the poorly controlled diabetic patients, their glycated CD36 levels were lower. These data were corroborated by in vitro studies demonstrating that increasing glucose concentrations reduced glycated protein levels (P < 0.05). Conclusions Our results demonstrate that CD36 expression is altered by hyperglycaemia in atherosclerotic patients.
引用
收藏
页码:854 / 862
页数:9
相关论文
共 25 条
[1]   CD36 and macrophages in atherosclerosis [J].
Collot-Teixeira, Sophie ;
Martin, Juliette ;
McDennott-Roe, Chris ;
Poston, Robin ;
McGregor, John Louis .
CARDIOVASCULAR RESEARCH, 2007, 75 (03) :468-477
[2]  
Esper RJ, 2008, ADV CARDIOL, V45, P17, DOI 10.1159/000115120
[3]   Stem cell transplantation reveals that absence of macrophage CD36 is protective against atherosclerosis [J].
Febbraio, M ;
Guy, E ;
Silverstein, RL .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2004, 24 (12) :2333-2338
[4]  
Feng JW, 2000, J LIPID RES, V41, P688
[5]   Macrophage-specific inhibition of NF-κB activation reduces foam-cell formation [J].
Ferreira, Valerie ;
van Dijk, Ko Willems ;
Groen, Albert K. ;
Vos, Rogier M. ;
van der Kaa, Jos ;
Gijbels, Marion J. J. ;
Havekes, Louis M. ;
Pannekoek, Hans .
ATHEROSCLEROSIS, 2007, 192 (02) :283-290
[6]   MECHANISMS OF DISEASE - THE PATHOGENESIS OF CORONARY-ARTERY DISEASE AND THE ACUTE CORONARY SYNDROMES .1. [J].
FUSTER, V ;
BADIMON, L ;
BADIMON, JJ ;
CHESEBRO, JH .
NEW ENGLAND JOURNAL OF MEDICINE, 1992, 326 (04) :242-250
[7]   PAS-IV, AN INTEGRAL MEMBRANE-PROTEIN OF MAMMARY EPITHELIAL-CELLS, IS RELATED TO PLATELET AND ENDOTHELIAL CELL-CD36 (GP-IV) [J].
GREENWALT, DE ;
WATT, KWK ;
SO, OY ;
JIWANI, N .
BIOCHEMISTRY, 1990, 29 (30) :7054-7059
[8]   A link between diabetes and atherosclerosis: Glucose regulates expression of CD36 at the level of translation [J].
Griffin, E ;
Re, A ;
Hamel, N ;
Fu, CZ ;
Bush, H ;
McCaffrey, T ;
Asch, AS .
NATURE MEDICINE, 2001, 7 (07) :840-846
[9]   Continued inhibition of atherosclerotic lesion development in long term Western diet fed CD36°/apoE° mice [J].
Guy, Ella ;
Kuchibhotla, Sai ;
Silverstein, Roy ;
Febbraio, Maria .
ATHEROSCLEROSIS, 2007, 192 (01) :123-130
[10]   Soluble CD36 in Plasma Is Increased in Patients With Symptomatic Atherosclerotic Carotid Plaques and Is Related to Plaque Instability [J].
Handberg, Aase ;
Skjelland, Mona ;
Michelsen, Annika E. ;
Sagen, Ellen Lund ;
Krohg-Sorensen, Kirsten ;
Russell, David ;
Dahl, Arve ;
Ueland, Thor ;
Oie, Erik ;
Aukrust, Pal ;
Halvorsen, Bente .
STROKE, 2008, 39 (11) :3092-3095