Adhesion molecules in cerebrovascular diseases -: Evidence for an inflammatory endothelial activation in cerebral large- and small-vessel disease

被引:87
作者
Fassbender, K
Bertsch, T
Mielke, O
Mühlhauser, F
Hennerici, M
机构
[1] Heidelberg Univ, Klinikum Mannheim, Dept Neurol, D-68135 Mannheim, Germany
[2] Heidelberg Univ, Klinikum Mannheim, Inst Clin Chem, D-68135 Mannheim, Germany
关键词
angiopathy; cell adhesion molecules; cerebrovascular disorders;
D O I
10.1161/01.STR.30.8.1647
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background and Purpose-Adhesion molecules mediate attachment and transendothelial migration of leukocytes as a critical step in pathogenesis of atherosclerosis. Their expression and release were comparatively investigated in patients with large- and small-vessel disease of the central nervous system. Methods-With immunological methods, serum concentrations of endothelial-derived adhesion molecules (soluble endothelial-leukocyte adhesion molecule [sE-selectin], soluble vascular-leukocyte adhesion molecule-1, and soluble intercellular adhesion molecule-1 [sICAM-1]) were quantified in patients with obstructive disease of extracranial (n=89) and intracranial (n=20) large-vessel disease and patients with subcortical vascular encephalopathy (n=64), a cerebral small-vessel disease. As controls, age- and sex-matched subjects without obstructive cerebrovascular disease (n=67) were studied. Results-We observed significantly increased serum concentrations of sE-selectin and sICAM-1 in patients with both obstructive disease of the large brain-supplying arteries and subcortical vascular encephalopathy. Interestingly, the highest levels were observed in intracranial macroangiopathy. Furthermore, concentrations of sICAM-1 and sE-selectin were significantly increased in current smokers but not in diabetic or hypertensive patients. Conclusions-The observation of elevated release of endothelial-derived adhesion molecules in both patients with stenoses of the large brain-supplying arteries and patients with subcortical vascular encephalopathy indicates that inflammatory endothelial activation and adhesion of leukocytes play similarly important roles in cerebral large- and small-vessel disease.
引用
收藏
页码:1647 / 1650
页数:4
相关论文
共 26 条
[1]   INFLAMMATION AND CORONARY-ARTERY DISEASE [J].
ALEXANDER, RW .
NEW ENGLAND JOURNAL OF MEDICINE, 1994, 331 (07) :468-469
[2]   Native low density lipoprotein-induced calcium transients trigger VCAM-1 and E-selectin expression in cultured human vascular endothelial cells [J].
Allen, S ;
Khan, S ;
Futwan-Al-Mohanna ;
Batten, P ;
Yacoub, M .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (05) :1064-1075
[3]   ENDOTHELIAL LEUKOCYTE ADHESION MOLECULE-1 - AN INDUCIBLE RECEPTOR FOR NEUTROPHILS RELATED TO COMPLEMENT REGULATORY PROTEINS AND LECTINS [J].
BEVILACQUA, MP ;
STENGELIN, S ;
GIMBRONE, MA ;
SEED, B .
SCIENCE, 1989, 243 (4895) :1160-1165
[4]  
CARLOS TM, 1994, BLOOD, V84, P2068
[5]   Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium [J].
Chappell, DC ;
Varner, SE ;
Nerem, RM ;
Medford, RM ;
Alexander, RW .
CIRCULATION RESEARCH, 1998, 82 (05) :532-539
[6]   Expression of inflammatory mediators and adhesion molecules in human atherosclerotic plaque [J].
DeGraba, TJ .
NEUROLOGY, 1997, 49 (05) :S15-S19
[7]   Impaired calcium regulation in subcortical vascular encephalopathy [J].
Eckert, A ;
Oster, M ;
Forstl, H ;
Hennerici, M ;
Muller, WE .
STROKE, 1997, 28 (07) :1351-1356
[8]   Focal expression of intercellular adhesion molecule-1 in the human carotid bifurcation [J].
Endres, M ;
Laufs, U ;
Merz, H ;
Kaps, M .
STROKE, 1997, 28 (01) :77-82
[9]   CIRCULATING SELECTIN-TYPE AND IMMUNOGLOBULIN-TYPE ADHESION MOLECULES IN ACUTE ISCHEMIC STROKE [J].
FASSBENDER, K ;
MOSSNER, R ;
MOTSCH, L ;
KISCHKA, U ;
GRAU, A ;
HENNERICI, M .
STROKE, 1995, 26 (08) :1361-1364
[10]   Soluble adhesion molecules reflect endothelial cell activation in ischemic stroke and in carotid atherosclerosis [J].
Frijns, CJM ;
Kappelle, LJ ;
vanGijn, J ;
Nieuwenhuis, HK ;
Sixma, JJ ;
Fijnheer, R .
STROKE, 1997, 28 (11) :2214-2218