Abstract
Galectin-3 is a β-galactoside-binding lectin which is important in cell proliferation and apoptotic regulation. Recently, serum galectin-3 has been shown to have prognostic value as a biomarker in heart failure. Encephalomyocarditis virus (EMCV) can cause severe myocarditis, congestive heart failure and dilated cardiomyopathy as well as encephalitis in various animals including mice. The pathophysiological role of galectin-3 in acute myocarditis following viral infection is not fully understood. The goal of this study is to determine the cardiac localization and the time-course of galectin-3 expression in heart failure after viral inoculation with EMCV. At 12, 24, 48, 96 hours, 7 and 10 days after intraperitoneal EMCV inoculation, animals were examined histologically and analyzed for the expression of galectin-3 and Iba1. Galectin-3 was up-regulated in degenerated fibrotic lesions of cardiac tissues 96 hours after viral inoculation and were followed by myocardial fibrosis. At the same time, Iba1 positive macrophages were observed within the inflammatory sites. A time-course correlation between the number of galectin-3 positive cells and the cardiac area of degenerated fibrotic lesions was detected—serum galectin-3 increased at 96 hours and correlated well with the number of cardiac galectin-3 positive cells. Our results indicate that galectin-3 expression may be a useful biomarker of cardiac fibrotic degeneration in acute myocarditis following viral infection. In addition, measuring serum galectin-3 levels might be an early diagnostic method for detecting cardiac degeneration in acute myocarditis.
Highlights
Galectins are a family of beta-galactoside-binding lectins
Representative photomicrographs of conventional hematoxylin and eosin (H&E) staining, Azan staining for fibrotic lesions, and immunohistochemistry for galectin-3 and Ionized calcium binding adaptor molecule 1 (Iba1) in heart tissues at 0, 12, 24, 48, 96 hours, 7 and 10 days after Encephalomyocarditis virus (EMCV)
We observed galectin-3 positive cells infiltration in this second heart failure model (Fig 5). This is the first study to analyze the relationship between cardiac localization and serum level of galectin-3 in an animal model for myocarditis after a virus inoculation
Summary
Galectins are a family of beta-galactoside-binding lectins. One member of this family, galectin, binds glycoconjugates and IgE on mammalian cell surfaces.[1]. A few galectin-3 positive cells were detected in cerebellum microlesions during the immediate-early phase of encephalitis—as early as 48h –after EMCV inoculation This findings indicate that galectin-3 expression may be a pivotal mediator between viral infection and encephalitis-induced neuronal degeneration in central nervous system, and that detection of galectin-3 might be an early diagnostic method for localized neuronal degeneration after virus infection. We hypothesize that analogous to viral-induced neuronal degeneration, increased galectin-3 levels may be a diagnostic biomarker for early myocardiac lesions. To test this hypothesis, we investigated the time-course of changes of cardiac and serum galectin-3 in the EMCV-infected mouse myocarditis model. We observed that galectin-3 expression may be a pivotal mediator of cardiac fibrotic degeneration in early phase of myocarditis following EMCV infection, and that detection of serum galectin-3 might be an early diagnostic biomarker for cardiac degeneration in acute myocarditis after virus infection
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
