Galectin-3 is expressed in the myocardium very early post-myocardial infarction

Document Type



Biological and Biomedical Sciences


Background: Galectin-3 (GAL-3) plays a regulatory role in several diverse biological processes and disease states. It is associated with heart failure and increased risk of death in a number of studies. We aim to study the direct effects of ischemia on GAL-3 levels in the heart very early in the course of events following myocardial infarction (MI).
Methods: Male C57B6/J mice were used for permanently ligating the left anterior descending artery of the heart to create ischemia/infarction in the anterior wall of left ventricle (LV). Heart samples were processed for immunohistochemical and immunofluorescent labeling, enzyme-linked immunosorbent assay, and quantitative reverse transcriptase polymerase chain reaction to identify GAL-3 levels in the heart during the first 24 h following MI.
Results: GAL-3 mRNA was significantly increased at 60min (P=.032), 4 h (P=.012), and 24 h (P=.00) post-MI groups in the infarcted LV as compared to sham. Thirty minutes post-MI GAL-3 mRNA is higher than the sham and almost reaching statistical significance (P=.056). GAL-3 protein was significantly increased in the LV at 30 min (P=.021), 60 min (P=.029), 4 h (P=.015), and 24 h (P=.01) post-MI compared to corresponding sham-operated mice. Plasma GAL-3 levels are also significantly raised at 24-h post-MI. GAL-3 is colocalized with cardiomyocytes and endothelial cells in the ischemic area of the LV. GAL-3 is also colocalized with hypoxia-inducible factor-1 alpha (HIF-1α).
Conclusions: We show for the first time that GAL-3 is increased at both transcriptional and translational levels in the LV in early ischemic period, which can possibly be a part of the prosurvival gene expression profile transcribed by HIF-1α. This is significant because it can help in understanding the mechanism of very early response of the myocardium following acute infarction and help devise ways to save the viable tissue before permanent damage sets in.

Publication (Name of Journal)

Cardiovascular Pathology