Multiple roles for MMPs and TIMPs in cerebral ischemia

GLIA - Tập 50 Số 4 - Trang 329-339 - 2005
Lee Anna Cunningham1, Monica K. Wetzel1, Gary A. Rosenberg1
1Departments of Neurosciences and Neurology, University of New Mexico School of Medicine, Albuquerque, New Mexico

Tóm tắt

AbstractMatrix metalloproteinases (MMPs) are matrix‐degrading enzymes involved in diverse homeostatic and pathological processes. Several MMPs are expressed within the CNS and serve important normal and pathological functions during development and adulthood. An early and major pathological effect of MMP activity after cerebral ischemia is opening of the blood‐brain barrier (BBB). More recent work demonstrates emerging roles for MMPs and their natural inhibitors, tissue inhibitors of metalloproteinases (TIMPs), in the regulation of neuronal cell death. In addition, MMPs and TIMPs are likely to play important roles during the repair phases of cerebral ischemia, particularly during angiogenesis and reestablishment of cerebral blood flow. This review attempts to elucidate how MMPs and TIMPs may provide detrimental or beneficial actions during the injury and repair processes after cerebral ischemia. These processes will have important implications for therapies using MMP inhibitors in stroke. © 2005 Wiley‐Liss, Inc.

Từ khóa


Tài liệu tham khảo

10.1161/01.STR.0000033932.34467.97

Apodaca G, 1990, Expression of metalloproteinases and metalloproteinase inhibitors by fetal astrocytes and glioma cells, Cancer Res, 50, 2322

10.1002/aja.1002000302

10.1006/geno.1994.1016

10.1074/jbc.270.24.14313

10.1002/glia.10255

10.1097/00004647-200012000-00007

10.1097/00001756-200109170-00050

10.1523/JNEUROSCI.21-19-07724.2001

10.1126/science.281.5381.1305

10.1523/JNEUROSCI.16-24-07910.1996

10.1242/jcs.00063

10.1038/35036374

10.1007/s000180050320

10.1016/S0167-4838(99)00279-4

10.1016/S0962-8924(01)02122-5

10.1097/01.WCB.0000091765.61714.30

10.1046/j.1471-4159.2002.01038.x

10.1074/jbc.M307051200

10.1002/(SICI)1098-1136(199912)28:3<183::AID-GLIA2>3.0.CO;2-3

10.1016/S0006-8993(03)02344-8

10.1016/S0166-2236(99)01401-0

10.1016/j.febslet.2004.03.070

10.1038/nrc745

10.1111/j.1750-3639.2000.tb00239.x

10.1016/0955-2235(95)00017-8

10.1111/j.1749-6632.1999.tb07765.x

10.1210/en.2003-0636

10.1097/00001756-199902050-00025

10.1083/jcb.141.7.1539

10.1097/00004647-200112000-00003

10.1159/000097229

10.1126/science.1073634

10.1172/JCI200421227

Hamann GF, 1999, Hemorrhagic transformation of cerebral infarction—possible mechanisms, Thromb Haemost, 82, 92

10.1161/01.STR.26.11.2120

10.1097/00004647-199611000-00036

10.1016/S0092-8674(00)80108-7

10.1093/brain/123.4.698

10.1073/pnas.0305755101

Hayashita‐Kinoh H, 2001, Membrane‐type 5 matrix metalloproteinase is expressed in differentiated neurons and regulates axonal growth, Cell Growth Differ, 12, 573

10.1097/00062752-200303000-00007

10.1097/00004647-199906000-00005

10.1021/bi020643m

10.1016/S0166-2236(02)02169-0

Issa R, 1999, Vascular endothelial growth factor and its receptor, KDR, in human brain tissue after ischemic stroke, Lab Invest, 79, 417

10.1002/1531-8249(20010201)49:2<230::AID-ANA43>3.0.CO;2-O

10.1046/j.1460-9568.2003.02876.x

10.1097/01.WCB.0000090680.07515.C8

Kang T, 2002, Activation of membrane‐type matrix metalloproteinase 3 zymogen by the proprotein convertase furin in the trans‐Golgi network, Cancer Res, 62, 675

10.1160/TH03-02-0070

10.1161/01.STR.25.9.1794

10.1007/BF00688633

10.1523/JNEUROSCI.23-10-04034.2003

10.1016/S0021-9258(17)37115-6

10.1126/science.1065057

10.1523/JNEUROSCI.4243-03.2004

10.1002/glia.10131

10.1055/s-0037-1616230

10.1161/01.STR.0000037675.97888.9D

10.1038/nrn1106

10.1023/A:1012493808790

Marti HH, 1999, Angiogenesis in ischemic disease, Thromb Haemost, 82, 44

10.1016/S0002-9440(10)64964-4

10.1038/sj.cdd.4400882

10.1523/JNEUROSCI.19-10-03809.1999

10.1523/JNEUROSCI.20-18-06879.2000

10.1016/0165-5728(96)00082-3

10.1186/1471-2210-1-7

10.1016/S1357-4310(00)01686-5

10.1016/S0960-9822(00)00038-5

10.1046/j.1471-4159.1998.70020721.x

10.1093/jnci/91.19.1678

Mitsiades N, 2001, Matrix metalloproteinase‐7‐mediated cleavage of Fas ligand protects tumor cells from chemotherapeutic drug cytotoxicity, Cancer Res, 61, 577

10.1161/01.STR.32.8.1759

10.1161/hs1201.99512

10.1161/01.CIR.0000046451.38849.90

10.1046/j.1523-1747.1998.00209.x

10.1152/ajpregu.1998.274.5.R1203

10.1097/00004647-199811000-00001

10.1042/bss0700201

10.1074/jbc.274.31.21491

10.1200/JCO.2000.18.5.1135

10.1523/JNEUROSCI.19-19-08464.1999

10.1016/S0960-9822(00)80113-X

10.1038/nm846

10.1523/JNEUROSCI.22-09-03504.2002

10.1038/386671a0

10.1046/j.0953-816x.2001.01838.x

10.1002/1097-4547(20000915)61:6<686::AID-JNR12>3.0.CO;2-7

10.1089/neu.1995.12.833

10.1177/1073858402238517

10.1002/glia.10108

10.1016/0006-8993(92)90681-X

10.1161/01.STR.29.10.2189

10.1016/S0006-8993(00)03294-7

Rosenberg GA, 2004, Matrix metalloproteinases in neuroinflammation and cerebral ischemia, Ernst Schering Res Found Workshop, 1

10.1002/stem.170237

10.1007/s004410050942

SeoD‐W LiH GuedezL WingfieldPT DiazT SalloumR WeiB‐Y Stetler‐StevensonWG.2003.Timp‐2 mediated inhibition of angiogenesis: An MMP‐independent mechanism. Cell114:171–180.

10.1146/annurev.cellbio.17.1.463

10.1002/glia.10266

10.1016/S1044-7431(02)00024-6

10.1002/1097-4547(20000715)61:2<212::AID-JNR12>3.0.CO;2-9

10.1161/01.RES.0000070112.80711.3D

10.1016/S0092-8674(00)81169-1

10.1097/01.WCB.0000040943.89393.c1

10.1016/0304-3940(91)90708-2

10.1111/j.1699-0463.1999.tb01521.x

10.1046/j.1460-9568.2003.02838.x

10.1023/B:APPT.0000038038.42809.e2

10.1038/35081571

10.1074/jbc.M000907200

10.1172/JCI9369

10.1074/jbc.M308708200