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Retraction notice to 'Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury' [Int. J. Cardiol. 163 (2013) 326-334]

Authors :
James McCormick
David S. Latchman
Richard A. Knight
Hisanori Suzuki
Samir Ounzain
Louis I.I. Saravolatz
Tiziano M. Scarabelli
Alessandro Mazzucco
Sean P. Barry
Christoph Thiemermann
Giuseppe Faggian
Anastasis Stephanou
Carol Chen-Scarabelli
Source :
International Journal of Cardiology
Publication Year :
2018

Abstract

Background IL-17A and IL-17F are pro-inflammatory cytokines which induce the expression of several cytokines, chemokines and matrix metalloproteinases (MMPs) in target cells. IL-17 cytokines have recently attracted huge interest due to their pathogenic role in diseases such as arthritis and inflammatory bowel disease although a role for IL-17 cytokines in myocardial infarction (MI) has not previously been described. Methods In vivo MI was performed by coronary artery occlusion in the absence or presence of a neutralizing IL-17 antibody for blocking IL-17 actions in vivo. IL-17 signaling was also assessed in isolated primary cardiomyocytes by Western blot, mRNA expression and immunostaining. Results Expression of IL-17A, IL-17F and the IL-17 receptor (IL-17RA) were all increased following MI. Expression of several IL-17 target genes, including Cxcl1, Cxcl2, IL-1β, iNOS and IL-6 was also upregulated following MI. In addition, IL-17A promoted the expression of Cxcl1 and IL-6 in isolated cardiomyocytes in a MAPK and PI(3)K-dependent manner. IL-17A and ischaemia/reperfusion (I/R) injury were found to have an additive effect on Cxcl1 expression, suggesting that IL-17 may enhance myocardial neutrophil recruitment during MI. Moreover, protein levels of both IL-17R and IL-17A were enhanced following in vivo MI. Finally, blocking IL-17 signaling in vivo reduced the levels of apoptotic cell death markers following in vivo MI. Conclusions These data imply that the expression of IL-17 cytokines and their receptor are elevated during myocardial I/R injury and may play a fundamental role in post infarct inflammatory and apoptotic responses.

Details

ISSN :
18741754
Volume :
274
Database :
OpenAIRE
Journal :
International journal of cardiology
Accession number :
edsair.doi.dedup.....370e08ebbd890d681c39626bf810b189