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Activation Systems for Latent Matrix Metalloproteinase-2 Are Upregulated Immediately After Focal Cerebral Ischemia

Authors
 Dae-Il Chang  ;  Naohisa Hosomi  ;  Gregory J del Zoppo  ;  Andrew P Mazarparallel  ;  Takeo Abumiya  ;  Ji-Hoe Heo  ;  Jacinta Lucero 
Citation
 JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Vol.23(12) : 1408-1419, 2003 
Journal Title
 JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM 
ISSN
 0271-678X 
Issue Date
2003
Abstract
During focal cerebral ischemia, matrix metalloproteinase-2 (MMP-2) can contribute to the loss of microvessel integrity within ischemic regions by degrading the basal lamina. MMP-2 is secreted in latent form (pro-MMP-2), but the activation of pro-MMP-2 in the ischemic territory has not been shown. Immunohistochemical and in situ hybridization studies of the expression of the direct activators of MMP-2, MT1-MMP and MT3-MMP, and the indirect activation system tissue plasminogen activator, urokinase (u-PA), its receptor (u-PAR), and its inhibitor PAI-1 after middle cerebral artery occlusion/reperfusion were undertaken in basal ganglia samples from 26 adolescent male baboons. The expressions of all three MMPs, u-PA, u-PAR, and PA1-1, but not tissue plasminogen activator, were increased from 1 hour after middle cerebral artery occlusion in the ischemic core. mRNA transcripts confirmed the increases in latent MMP-2, u-PA, u-PAR, and PAI-1 antigen very early after middle cerebral artery occlusion. The expression patterns are consistent with secretion of pro-MMP-2 and its activators in the ischemic core, perhaps from separate cell compartments. The rapid and coordinate appearance of pro-MMP-2 and its activation apparatus suggest that in the primate striatum this protease may participate in matrix injury during focal cerebral ischemia.
Full Text
http://www.nature.com/jcbfm/journal/v23/n12/abs/9591490a.html
DOI
10.1097/01.WCB.0000091765.61714.30
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
Yonsei Authors
Heo, Ji Hoe(허지회) ORCID logo https://orcid.org/0000-0001-9898-3321
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/114145
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