Different signalling in infarcted and non-infarcted areas of rat failing hearts: A role of necroptosis and inflammation
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F19%3A00510386" target="_blank" >RIV/67985823:_____/19:00510386 - isvavai.cz</a>
Result on the web
<a href="https://doi.org/10.1111/jcmm.14536" target="_blank" >https://doi.org/10.1111/jcmm.14536</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1111/jcmm.14536" target="_blank" >10.1111/jcmm.14536</a>
Alternative languages
Result language
angličtina
Original language name
Different signalling in infarcted and non-infarcted areas of rat failing hearts: A role of necroptosis and inflammation
Original language description
Necroptosis has been recognized in heart failure (HF). In this study, we investigated detailed necroptotic signalling in infarcted and non-infarcted areas separately and its mechanistic link with main features of HF. Post-infarction HF in rats was induced by left coronary occlusion (60 minutes) followed by 42-day reperfusion. Heart function was assessed echocardiographically. Molecular signalling and proposed mechanisms (oxidative stress, collagen deposition and inflammation) were investigated in whole hearts and in subcellular fractions when appropriate. In post-infarction failing hearts, TNF and pSer229-RIP3 levels were comparably increased in both infarcted and non-infarcted areas. Its cytotoxic downstream molecule p-MLKL, indicating necroptosis execution, was detected in infarcted area. In non-infarcted area, despite increased pSer229-RIP3, p-MLKL was present in neither whole cells nor the cell membrane known to be associated with necroptosis execution. Likewise, increased membrane lipoperoxidation and NOX2 levels unlikely promoted pro-necroptotic environment in non-infarcted area. Collagen deposition and the inflammatory csp-1-IL-1 beta axis were active in both areas of failing hearts, while being more pronounced in infarcted tissue. Although apoptotic proteins were differently expressed in infarcted and non-infarcted tissue, apoptosis was found to play an insignificant role. p-MLKL-driven necroptosis and inflammation while inflammation only (without necroptotic cell death) seem to underlie fibrotic healing and progressive injury in infarcted and non-infarcted areas of failing hearts, respectively. Upregulation of pSer229-RIP3 in both HF areas suggests that this kinase, associated with both necroptosis and inflammation, is likely to play a dual role in HF progression.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30201 - Cardiac and Cardiovascular systems
Result continuities
Project
<a href="/en/project/NV15-27735A" target="_blank" >NV15-27735A: Progression of chronic heart failure and cardiorenal syndrome in hypertensive rats after myocardial infarction: role of epoxyeicosatrienoic acids.</a><br>
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2019
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Journal of Cellular and Molecular Medicine
ISSN
1582-4934
e-ISSN
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Volume of the periodical
23
Issue of the periodical within the volume
9
Country of publishing house
GB - UNITED KINGDOM
Number of pages
13
Pages from-to
6429-6441
UT code for WoS article
000484153100001
EID of the result in the Scopus database
2-s2.0-85071494302