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Anti-apoptotic role...
Anti-apoptotic role for C1 inhibitor in ischemia/reperfusion-induced myocardial cell injury.
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Fu, Jinrong (author)
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Lin, Guosheng (author)
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Wu, Zhiwei (author)
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Ceng, Bin (author)
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Wu, Yanxia (author)
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Liang, Gong (author)
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Qin, Gangjian (author)
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Li, Jinan (author)
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Chiu, Isaac (author)
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Liu, Dongxu (author)
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- Elsevier BV, 2006
- 2006
- English.
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In: Biochemical and Biophysical Research Communications - BBRC. - : Elsevier BV. - 0006-291X .- 1090-2104. ; 349:2, s. 504-12
- Related links:
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
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- Complement activation augments myocardial cell injury and apoptosis during ischemia/reperfusion (I/R), whereas complement system inhibition with C1 inhibitor (C1INH), a serine protease inhibitor, exerts markedly cardioprotective effects. Our recent data demonstrate that C1INH prevents vascular endothelial cell apoptosis and a "modified" form of the reactive center loop-cleaved, inactive C1INH (iC1INH) plays an anti-inflammatory role in endotoxin shock. The aim of this study was to determine whether C1INH protects against myocardial cell injury via an anti-apoptotic activity or anti-inflammatory effect. In a rat model of acute myocardial infarction (AMI) induced by I/R, administration of C1INH protected against cardiomyocytic apoptosis via normalization of ratio of the Bcl-2/Bax expression in the myocardial infarct area. C1INH improved parameters of cardiac function and hemodynamics and reduced myocardial infarct size (MIS). In addition, myocardial and blood myeloperoxidase (MPO) activity, a marker of neutrophil infiltration, was decreased by treatment of C1INH. In cultured H9c2 rat cardiomyocytic cells, C1INH blocked hypoxia/reoxygenation-induced apoptosis in the absence of sera associated with inhibition of cytochrome c translocation and suppression of caspase-3 activation. The proportion of Bcl-2/Bax expression induced by hypoxia/reoxygenation was reversed by C1INH. Importantly, iC1INH also revealed these similar effects, indicating that C1INH has a direct anti-apoptotic activity. Therefore, these studies support the hypothesis that C1INH, in addition to inhibition of activation of the complement and contact systems, improves outcome in I/R-mediated myocardial cell injury via an anti-apoptotic activity independent of serine protease inhibitory activity.
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- By the author/editor
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Fu, Jinrong
-
Lin, Guosheng
-
Wu, Zhiwei
-
Ceng, Bin
-
Wu, Yanxia
-
Liang, Gong
-
show more...
-
Qin, Gangjian
-
Li, Jinan
-
Chiu, Isaac
-
Liu, Dongxu
-
show less...
- Articles in the publication
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Biochemical and ...
- By the university
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Umeå University