Endothelin-1 and monocyte chemoattractant protein-1 modulation in ischemia and human brain-derived endothelial cell cultures

被引:57
作者
Chen, P
Shibata, M
Zidovetzki, R
Fisher, M
Zlokovic, BV
Hofman, FM
机构
[1] Univ So Calif, Sch Med, Dept Pathol, Los Angeles, CA 90033 USA
[2] Univ Calif Riverside, Dept Cell Biol & Neurosci, Riverside, CA 92521 USA
[3] Univ Calif Irvine, Dept Neurol, Irvine, CA 92868 USA
[4] Univ Rochester, Sch Med, Inst Biomed Sci, Ctr Aging & Dev Biol,Div Neurovasc Biol, Rochester, NY 14642 USA
关键词
endothelin; MCP-1; cerebral ischemia; macrophage; endothelium;
D O I
10.1016/S0165-5728(01)00280-6
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Brain tissue damage due to ischemia/reperfusion has been shown to be caused, in part, by activated macrophages infiltrating into the post-ischemic brain. Using the Middle Cerebral Artery Occlusion (MCAO) mouse model, this study demonstrated that, in vivo, bath endothelin-1 (Et-1), a potent vasoconstrictor, and the macrophage chemokine, monocyte chemoattractant factor-1 (MCP-1) are induced in ischemia. Further studies, using human brain-derived endothelial cells (CNS-EC), showed that in vitro, Et-1 can directly stimulate MCP-1 mRNA expression and MCP-1 protein; and this Et-1-induced MCP-1 production is mediated by the ETA receptor. Inflammatory cytokines, tumor necrosis factor alpha and interleukin-1 beta, functioned additively and synergistically, respectively, with Et-1 to increase this MCP-1 production. Partial elucidation of the signal transduction pathways involved in Et-1-induced MCP-1 production demonstrated that protein kinase C-, but not cAMP-dependent pathways are involved. These data demonstrate that Et-1 functioning as an inflammatory peptide, increased levels of MCP-1, suggesting a mechanism for chemokine regulation during ischemia/reperfusion injury. (C) 2001 Published by Elsevier Science B.V.
引用
收藏
页码:62 / 73
页数:12
相关论文
共 62 条
[1]  
BAGGIOLINI M, 1994, ADV IMMUNOL, V55, P97
[2]  
BARONE FC, 1995, J CARDIOVASC PHARM, V26, pS404
[3]   ENDOTHELIN LEVELS INCREASE IN RAT FOCAL AND GLOBAL-ISCHEMIA [J].
BARONE, FC ;
GLOBUS, MYT ;
PRICE, WJ ;
WHITE, RF ;
STORER, BL ;
FEUERSTEIN, GZ ;
BUSTO, R ;
OHLSTEIN, EH .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1994, 14 (02) :337-342
[4]   Endothelin receptor antagonist preserves microvascular perfusion and reduces ischemic brain damage following permanent focal ischemia [J].
Dawson, DA ;
Sugano, H ;
McCarron, RM ;
Hallenbeck, JM ;
Spatz, M .
NEUROCHEMICAL RESEARCH, 1999, 24 (12) :1499-1505
[5]   HIGH PLASMA-LEVELS OF ENDOTHELIN-1 AND ATRIAL-NATRIURETIC-PEPTIDE IN PATIENTS WITH ACUTE ISCHEMIC STROKE [J].
ESTRADA, V ;
TELLEZ, MJ ;
MOYA, J ;
FERNANDEZDURANGO, R ;
EGIDO, J ;
CRUZ, AF .
AMERICAN JOURNAL OF HYPERTENSION, 1994, 7 (12) :1085-1089
[6]   Endothelial cell responses to hypoxic stress [J].
Faller, DV .
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 1999, 26 (01) :74-84
[7]   PEPTIDIC ENDOTHELIN-1 RECEPTOR ANTAGONIST, BQ-123, AND NEUROPROTECTION [J].
FEUERSTEIN, G ;
GU, JL ;
OHLSTEIN, EH ;
BARONE, FC ;
YUE, TL .
PEPTIDES, 1994, 15 (03) :467-469
[8]  
FEUERSTEIN GZ, 1994, CEREBROVAS BRAIN MET, V6, P341
[9]  
FLORY CM, 1993, LAB INVEST, V69, P396
[10]  
FURIE MB, 1995, AM J PATHOL, V146, P1287