Increased gelatinase A (MMP-2) and gelatinase B (MMP-9) activities in human brain after focal ischemia

被引:263
作者
Clark, AW
Krekoski, CA
Bou, SS
Chapman, KR
Edwards, DR
机构
[1] Univ Calgary, Dept Pathol, Calgary, AB T2N 4N1, Canada
[2] Univ Calgary, Dept Clin Neurosci, Calgary, AB, Canada
[3] Univ Calgary, Neurosci Res Grp, Calgary, AB, Canada
[4] Univ Calgary, Dept Med Biochem, Calgary, AB, Canada
关键词
cerebral ischemia; stroke; matrix metalloproteinase; gelatinase A; gelatinase B; MMP-2; MMP-9;
D O I
10.1016/S0304-3940(97)00859-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Matrix metalloproteinases (MMPs) are involved in remodelling extracellular matrix. Gelatinase B (MMP-9) is an inducible 92 kDa MMP expressed by neutrophils, microglia, and endothelial cells. Gelatinase A (MMP-2) is a 72 kDa MMP, constitutively expressed in brain. Elevated MMP activity has been linked to various pathologic conditions, and the therapeutic benefit of MMP inhibitors is under study in a few experimental models. Using gelatin zymography, we have compared activities of these MMPs in infarcted and matched non-infarcted cerebral tissue from eight subjects dying at intervals of less than 2 h to several years after a stroke. Gelatinase B activity was markedly elevated in the infarcted tissue at two days post-infarction, and remained elevated in cases dying months after the event. Increases in gelatinase A activity were subtle at 2-5 days; they were marked and significant in cases dying at 4 months and later. The findings indicate distinct temporal profiles of post-ischemic gelatinase activity in human brain, with earlier but equally persistent elevation in gelatinase B when compared to gelatinase A. (C) 1997 Elsevier Science Ireland Ltd.
引用
收藏
页码:53 / 56
页数:4
相关论文
共 24 条
[1]   Dynamics of polymorphonuclear leukocyte accumulation in acute cerebral infarction and their correlation with brain tissue damage [J].
Akopov, SE ;
Simonian, NA ;
Grigorian, GS .
STROKE, 1996, 27 (10) :1739-1743
[2]   PROTEASE PRODUCTION BY CULTURED MICROGLIA - SUBSTRATE GEL ANALYSIS AND IMMOBILIZED MATRIX DEGRADATION [J].
COLTON, CA ;
KERI, JE ;
CHEN, WT ;
MONSKY, WL .
JOURNAL OF NEUROSCIENCE RESEARCH, 1993, 35 (03) :297-304
[3]   POLYMORPHONUCLEAR LEUKOCYTES IN ISCHEMIC VASCULAR-DISEASE [J].
FISHER, TC ;
MEISELMANN, HJ .
THROMBOSIS RESEARCH, 1994, 74 :S21-S34
[4]   Hemorrhagic transformation and microvascular integrity during focal cerebral ischemia/reperfusion [J].
Hamann, GF ;
Okada, Y ;
delZoppo, GJ .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1996, 16 (06) :1373-1378
[5]   MICROVASCULAR BASAL LAMINA ANTIGENS DISAPPEAR DURING CEREBRAL-ISCHEMIA AND REPERFUSION [J].
HAMANN, GF ;
OKADA, Y ;
FITRIDGE, R ;
DELZOPPO, GJ .
STROKE, 1995, 26 (11) :2120-2126
[6]  
HERRON GS, 1986, J BIOL CHEM, V261, P2810
[7]   Role of laminin in matrix induction of macrophage urokinase-type plasminogen activator and 92-kDa metalloproteinase expression [J].
Khan, KMF ;
Falcone, DJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (13) :8270-8275
[8]   QUANTITATIVE ZYMOGRAPHY - DETECTION OF PICOGRAM QUANTITIES OF GELATINASES [J].
KLEINER, DE ;
STETLERSTEVENSON, WG .
ANALYTICAL BIOCHEMISTRY, 1994, 218 (02) :325-329
[9]   Relating matrix metalloproteinase structure to function: Why the ''hemopexin'' domain? [J].
Murphy, G ;
Knauper, V .
MATRIX BIOLOGY, 1997, 15 (8-9) :511-518
[10]   ISCHEMIC CEREBRAL EDEMA - REVIEW [J].
OBRIEN, MD .
STROKE, 1979, 10 (06) :623-628