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Mineralocorticoid receptor antagonists modulate galectin-3 and interleukin-33/ST2 signaling in left ventricular systolic dysfunction after acute myocardial infarction

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dc.contributor.authorLax Pérez, Antonio Manuel
dc.contributor.authorSánchez Mas, Jesús
dc.contributor.authorAsensio Lopez, Maria del Carmen
dc.contributor.authorFernandez del Palacio, Maria J
dc.contributor.authorCaballero, Luis
dc.contributor.authorGarrido, Iris P
dc.contributor.authorPastor Pérez, Francisco J
dc.contributor.authorJanuzzi, James L
dc.contributor.authorPascual Figal, Domingo A
dc.contributor.departmentMedicina
dc.date.accessioned2024-07-15T11:19:09Z
dc.date.available2024-07-15T11:19:09Z
dc.date.issued2015-01
dc.description© 2015 American College of Cardiology Foundation. This document is the Published version of a Published Work that appeared in final form in JACC: Heart Failure. To access the final edited and published work see https://doi.org/10.1016/j.jchf.2014.07.015
dc.description.abstractObjectives: This study aimed to evaluate the specific role of the 2 available mineralocorticoid receptor antagonists (MRAs), eplerenone and spironolactone, on the modulation of galectin-3 (Gal-3) and interleukin (IL)-33/ST2 signaling in an experimental model of left ventricular systolic dysfunction after acute myocardial infarction (MI). Background: The molecular mechanisms of benefits of MRAs in patients with left ventricular systolic dysfunction after MI not well understood. Methods: MI and left ventricular systolic dysfunction were induced by permanent ligation of the anterior coronary artery in 45 male Wistar rats, randomly assigned to no therapy (MI group, n = 15) or to receive MRAs (100 mg/kg/day) for 4 weeks; either eplerenone (n = 15) or spironolactone (n = 15) was used. A sham group was used as a control (n = 8). Elements of the pathway for Gal-3 including transforming growth factor (TGF)-β and SMAD3, as well as that for IL-33/ST2 (including IL-33 and soluble ST2 [sST2]) were analyzed in the infarcted and noninfarcted myocardium by quantitative real-time reverse transcription polymerase chain reaction. Expression of markers of fibrosis (collagen types I and III, tissue inhibitor of metalloproteinase-1) and inflammation (IL-6, tumor necrosis factor-α, monocyte chemotactic protein-1) was also examined. Results: In the infarcted myocardium, compared with sham animals, the MI group had higher concentrations of Gal-3, TGF-β, SMAD3, IL-33, and sST2, as well as higher concentrations of markers of fibrosis and inflammation. Treatment with MRAs down-regulated Gal-3, TGF-β, and SMAD3 and enhanced IL-33/ST2 signaling with lower expression of sST2; protective IL-33 up-regulation was unaffected by MRAs. Modulation of Gal-3 and IL-33/ST2 signaling induced by MRAs correlated with lower expression levels of fibrosis and inflammatory markers. No differences were found between eplerenone and spironolactone. In the noninfarcted myocardium, compared with sham animals, the MI group exhibited a higher expression of Gal-3 and IL-33, but no signs of inflammation or fibrosis were observed; in the presence of MRAs, IL-33 expression was significantly up-regulated, but Gal-3 was unaffected. Conclusions: MRAs play a pivotal role in the Gal-3 and IL-33/ST2 modulation in post-MI cardiac remodeling.es
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dc.format.extent9es
dc.identifier.citationJACC: Heart Failure. 2015, Vol. 3 (1), pp. 50–58
dc.identifier.doihttps://doi.org/10.1016/j.jchf.2014.07.015
dc.identifier.issnPrint: 2213-1779
dc.identifier.issnElectronic: 2213-1787
dc.identifier.urihttp://hdl.handle.net/10201/143089
dc.languageenges
dc.publisherElsevier
dc.relationThis study was supported in part by grant 11857/PI/09 from Fundación Séneca, 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://www.sciencedirect.com/science/article/pii/S2213177914003874?via%3Dihub#ack0010
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectEplerenone
dc.subjectHeart failure
dc.subjectMyocardial infarction
dc.subjectRemodeling
dc.subjectSpironolactone
dc.titleMineralocorticoid receptor antagonists modulate galectin-3 and interleukin-33/ST2 signaling in left ventricular systolic dysfunction after acute myocardial infarctiones
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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