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Rapid Differential Endogenous Plasminogen Activator Expression After Acute Middle Cerebral Artery Occlusion

Authors
 Naohisa Hosomi  ;  Jacinta Lucero  ;  Ji Hoe Heo  ;  James A. Koziol  ;  Brian R. Copeland  ;  Gregory J. del Zoppo 
Citation
 STROKE, Vol.32(6) : 1341-1348, 2001 
Journal Title
 STROKE 
ISSN
 0039-2499 
Issue Date
2001
Keywords
basal ganglia ; cerebral ischemia ; focal ; microcirculation ; plasminogen activators ; tissue plasminogen activator ; baboons
Abstract
BACKGROUND AND PURPOSE: During focal cerebral ischemia, the microvascular matrix (ECM), which participates in microvascular integrity, is degraded and lost when neurons are injured. Loss of microvascular basal lamina antigens coincides with rapid expression of select matrix metalloproteinases (MMPs). Plasminogen activators (PAs) may also play a role in ECM degradation by the generation of plasmin or by MMP activation. METHODS: The endogenous expressions of tissue-type plasminogen activator (tPA), urokinase (uPA), and PA inhibitor-1 (PAI-1) were quantified in 10-microm frozen sections from ischemic and matched nonischemic basal ganglia and in the plasma of 34 male healthy nonhuman primates before and after middle cerebral artery occlusion (MCA:O). RESULTS: Within the ischemic basal ganglia, tissue uPA activity and antigen increased significantly within 1 hour after MCA:O (2P<0.005). tPA activity transiently decreased 2 hours after MCA:O (2P=0.01) in concert with an increase in PAI-1 antigen (2P=0.001) but otherwise did not change. The transient decrease in free tPA antigen was marked by an increase in the tPA-PAI-1 complex (2P<0.001). No significant relations to neuronal injury or intracerebral hemorrhage were discerned. CONCLUSIONS: The rapid increase in endogenous PA activity is mainly due to significant increases in uPA, but not tPA, within the ischemic basal ganglia after MCA:O. This increase and an increase in PAI-1 coincided with latent MMP-2 generation and microvascular ECM degeneration but not neuronal injury.
Files in This Item:
T200103675.pdf Download
DOI
10.1161/​01.STR.32.6.1341
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/22282913/143055
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