Sökning: onr:"swepub:oai:DiVA.org:umu-41176" >
Anti-apoptotic role...
Anti-apoptotic role for C1 inhibitor in ischemia/reperfusion-induced myocardial cell injury.
- Artikel/kapitelEngelska2006
Förlag, utgivningsår, omfång ...
-
Elsevier BV,2006
-
printrdacarrier
Nummerbeteckningar
-
LIBRIS-ID:oai:DiVA.org:umu-41176
-
https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-41176URI
-
https://doi.org/10.1016/j.bbrc.2006.08.065DOI
Kompletterande språkuppgifter
-
Språk:engelska
-
Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
-
Ämneskategori:ref swepub-contenttype
-
Ämneskategori:art swepub-publicationtype
Anmärkningar
-
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.
Biuppslag (personer, institutioner, konferenser, titlar ...)
-
Lin, Guosheng
(författare)
-
Wu, Zhiwei
(författare)
-
Ceng, Bin
(författare)
-
Wu, Yanxia
(författare)
-
Liang, Gong
(författare)
-
Qin, Gangjian
(författare)
-
Li, Jinan
(författare)
-
Chiu, Isaac
(författare)
-
Liu, Dongxu
(författare)
Sammanhörande titlar
-
Ingår i:Biochemical and Biophysical Research Communications - BBRC: Elsevier BV349:2, s. 504-120006-291X1090-2104
Internetlänk
Hitta via bibliotek
Till lärosätets databas
- Av författaren/redakt...
-
Fu, Jinrong
-
Lin, Guosheng
-
Wu, Zhiwei
-
Ceng, Bin
-
Wu, Yanxia
-
Liang, Gong
-
visa fler...
-
Qin, Gangjian
-
Li, Jinan
-
Chiu, Isaac
-
Liu, Dongxu
-
visa färre...
- Artiklar i publikationen
-
Biochemical and ...
- Av lärosätet
-
Umeå universitet