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Modulation of IL-33/ST2 system in postinfarction heart failure: correlation with cardiac remodelling markers

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dc.contributor.authorSánchez Mas, Jesús
dc.contributor.authorLax Pérez, Antonio Manuel
dc.contributor.authorAsensio López, María del Carmen
dc.contributor.authorFernández del Palacio, María J
dc.contributor.authorCaballero, Luis
dc.contributor.authorSantarelli, Giorgia
dc.contributor.authorJanuzzi, James L
dc.contributor.authorPascual Figal, Domingo A
dc.contributor.departmentMedicina
dc.date.accessioned2024-07-15T11:33:41Z
dc.date.available2024-07-15T11:33:41Z
dc.date.issued2014-07
dc.description© 2014 Stichting European Society for Clinical Investigation Journal Foundation. This document is the Published version of a Published Work that appeared in final form inEuropean Journal of Clinical Investigation. To access the final edited and published work see https://doi.org/10.1111/eci.12282
dc.description.abstractBackground: Interleukin (IL)-33 and sST2 are molecules with an opposite pathophysiologic implications in the myocardial response after acute myocardial infarction (AMI). Both may be a target for therapeutic interventions. The kinetics of IL-33 and sST2 expression in infarcted myocardium and their correlation with the ongoing processes of fibrosis, inflammation and apoptosis remains poorly defined. Materials and methods: Fifty Wistar rats underwent left anterior descending coronary artery surgical ligation and were sacrificed at 1, 2, 4, 12 or 24 weeks post-AMI. A sham-operated group was also included. The mRNA cardiac expression levels of IL-33, sST2, fibrosis markers, inflammatory markers and apoptosis markers were assessed by RT-PCR. The protein expression of IL-33 was also measured by Western blotting. Results: The mRNA levels of IL-33 and sST2 were upregulated in the infarcted myocardium during the first week after AMI. However, while IL-33 levels remained elevated during the first 12 weeks post-AMI, sST2 levels showed a marked drop at 4 weeks. IL-33 protein expression showed a similar kinetic than mRNA expression. The expression of sST2 positively correlated with cardiac gene expression of inflammatory and fibrosis markers. However, the IL-33 level did not correlate with these cardiac remodelling markers. No correlation of sST2 with apoptosis markers was observed. Conclusion: After AMI, expression of sST2 is rapidly upregulated during the first 4 weeks and, in contrast to IL-33, its levels correlated with the ongoing processes of fibrosis and inflammation. These findings suggest differential regulation of IL33 and sST2. Therapeutic modulation of early sST2 expression may be of greater importance to prevent adverse remodelling after AMI.es
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dc.format.extent9es
dc.identifier.citationEuropean Journal of Clinical Investigation, 2014, Vol. 44, Issue 7, pp. 643-651
dc.identifier.doihttps://doi.org/10.1111/eci.12282
dc.identifier.issnPrint: 0014-2972
dc.identifier.issnElectronic: 1365-2362
dc.identifier.urihttp://hdl.handle.net/10201/143095
dc.languageenges
dc.publisherWiley
dc.relationThis study was supported in part by Grant 11857/PI/09 from Fundaci on S eneca, Murcia, Spain; by Grant PS09/02106 from the Ministerio de Sanidad, Madrid, Spain; and by the national network of investigation in cardiovascular diseases RD12/ 0042/0049.es
dc.relation.publisherversionhttps://onlinelibrary.wiley.com/doi/full/10.1111/eci.12282
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectAcute myocardial infarctiones
dc.subjectCardiac remodellinges
dc.subjectInterleukines
dc.subjectST2es
dc.titleModulation of IL-33/ST2 system in postinfarction heart failure: correlation with cardiac remodelling markerses
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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