open access

Vol 24, No 2 (2017)
Original articles — Basic science and experimental cardiology
Published online: 2016-10-17
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Preliminary study of beta-blocker therapy on modulation of interleukin-33/ST2 signaling during ventricular remodeling after acute myocardial infarction

Jinggang Xia, Yang Qu, Chunlin Yin, Dong Xu
DOI: 10.5603/CJ.a2016.0096
·
Pubmed: 27748502
·
Cardiol J 2017;24(2):188-194.

open access

Vol 24, No 2 (2017)
Original articles — Basic science and experimental cardiology
Published online: 2016-10-17

Abstract

Background: This study aimed to evaluate the role of b-blocker therapy on modulating interleukin (IL)-33/ST2 (interleukin-1 receptor-like 1) signaling during ventricular remodeling related to heart failure (HF) after acute myocardial infarction (AMI).

Methods: Sprague-Dawley rats that survived surgery to induce AMI were randomly divided into the placebo group and the b-blocker treatment group. A sham group was used as a control. Left ventricular (LV) function variables, the myocardial infarct size, fibrosis and IL-33/ST2 protein expression was measured.

Results: Compared with the placebo group, b-blocker treatment significantly improved LV function and reduced infarct size (p < 0.05). There was higher protein expression of IL-33 (p < 0.05) and sST2 (p < 0.05), as well as higher expression of fibrosis (p < 0.05), compared to the sham group. Notably, the high expression of cardioprotective IL-33 was not affected by b-blocker treatment (p > 0.05), however, treatment with b-blocker enhanced IL-33/ST2 signaling, with lower expression of sST2 (p < 0.05) and significantly attenuated fibrosis (p < 0.05).

Conclusions: Our study suggested that b-blocker therapy might play a beneficial role in the modula­tion of IL-33/ST2 signaling during ventricular remodeling. These results may be helpful in identifying IL-33/ST2 systems as putative b-blocker targets at an early stage after AMI. (Cardiol J 2017; 24, 2: 188–194)

Abstract

Background: This study aimed to evaluate the role of b-blocker therapy on modulating interleukin (IL)-33/ST2 (interleukin-1 receptor-like 1) signaling during ventricular remodeling related to heart failure (HF) after acute myocardial infarction (AMI).

Methods: Sprague-Dawley rats that survived surgery to induce AMI were randomly divided into the placebo group and the b-blocker treatment group. A sham group was used as a control. Left ventricular (LV) function variables, the myocardial infarct size, fibrosis and IL-33/ST2 protein expression was measured.

Results: Compared with the placebo group, b-blocker treatment significantly improved LV function and reduced infarct size (p < 0.05). There was higher protein expression of IL-33 (p < 0.05) and sST2 (p < 0.05), as well as higher expression of fibrosis (p < 0.05), compared to the sham group. Notably, the high expression of cardioprotective IL-33 was not affected by b-blocker treatment (p > 0.05), however, treatment with b-blocker enhanced IL-33/ST2 signaling, with lower expression of sST2 (p < 0.05) and significantly attenuated fibrosis (p < 0.05).

Conclusions: Our study suggested that b-blocker therapy might play a beneficial role in the modula­tion of IL-33/ST2 signaling during ventricular remodeling. These results may be helpful in identifying IL-33/ST2 systems as putative b-blocker targets at an early stage after AMI. (Cardiol J 2017; 24, 2: 188–194)

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Keywords

beta-blocker, IL-33/ST2, ventricular remodeling, acute myocardial infarction

About this article
Title

Preliminary study of beta-blocker therapy on modulation of interleukin-33/ST2 signaling during ventricular remodeling after acute myocardial infarction

Journal

Cardiology Journal

Issue

Vol 24, No 2 (2017)

Pages

188-194

Published online

2016-10-17

DOI

10.5603/CJ.a2016.0096

Pubmed

27748502

Bibliographic record

Cardiol J 2017;24(2):188-194.

Keywords

beta-blocker
IL-33/ST2
ventricular remodeling
acute myocardial infarction

Authors

Jinggang Xia
Yang Qu
Chunlin Yin
Dong Xu

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