title: Galectin-3 is expressed in the myocardium very early post-myocardial infarction.
abstract: 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.
authors.affiliation: Department of Biological and Biomedical Sciences, Agha Khan University, Stadium Road, Karachi 74800, Pakistan. Electronic address: satwat.hashmi@aku.edu.
authors.forename: Satwat
authors.initials: S
authors.lastname: Hashmi
authors.affiliation: Department of Pathology, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates. Electronic address: suhaila@uaeu.ac.ae.
authors.forename: Suhail
authors.initials: S
authors.lastname: Al-Salam
mesh_terms: D000818:Animals; D019938:Cyclin D1 / Q000378:metabolism; D004195:Disease Models, Animal; D004562:Electrocardiography; D042783:Endothelial Cells / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005455:Fluorescent Antibody Technique; D037502:Galectin 3 / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D006352:Heart Ventricles / Q000378:metabolism* / Q000473:pathology; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D008810:Mice, Inbred C57BL; D009203:Myocardial Infarction / Q000097:blood / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D014158:Transcription, Genetic; D015854:Up-Regulation
chemical_list: C530105:Ccnd1 protein, mouse; D037502:Galectin 3; C497443:Hif1a protein, mouse; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; C485095:Lgals3 protein, mouse; D012333:RNA, Messenger; D019938:Cyclin D1
keywords: Acute myocardial infarction; Galectin 3; Heart