Why the study?
Does Interleukin-22 deletion affect cardiac remodeling and promote cardiac rupture after acute myocardial infarction in mice?
Does Interleukin-22 deletion affect cardiac remodeling and promote cardiac rupture after acute myocardial infarction in mice?
IL-22 deletion promotes cardiac rupture after acute myocardial infarction in a mouse model, suggesting a protective role for IL-22 in post-infarction cardiac remodeling.
Background: Interleukin-22 (IL-22) is a member of the IL-10 cytokine family, which mainly targets epithelial cells and does not target immune cells. Although it has been shown that IL-22 play roles in tissue protection and wound repair, little is known about the role of IL-22 in the pathogenesis of cardiac remodeling after acute myocardial infarction (AMI). In the present study, we aimed to determine whether IL-22 could be expressed in the hearts and affect the cardiac remodeling after AMI in mice. Purpose: We investigated the role of IL-22 in cardiac remodeling after AMI in mice. Methods: AMI was produced by permanent ligation of the left coronary artery in wild type mice and IL-22 KO mice. The infarct size was estimated by evans blue dye and triphenyltetrazolium chloride staining. We evaluated the STAT3 activation in the heart by western blot analysis and Immunostaining for phospho-STAT3. Expressions of IL-22, IL-22 receptor subunit alpha 1 (IL-22RA1), IL-22 binding protein (IL-22BP), and matrix metalloproteinases (MMPs) were measured by real-time PCR analysis.
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Yamamoto et al. (2018) studied this question.
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