Galectin-3: A cardiomyocyte antiapoptotic mediator at 24-hour post myocardial infarction

Suhail Al-Salam, Satwat Hashmi, Govindan S. Jagadeesh, Saeed Tariq

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)

Abstract

Background/Aims: Galectin 3 (GAL-3) is a beta galactoside binding lectin that has different roles in normal and pathophysiological conditions. GAL-3 has been associated with heart failure and was linked to increased risk of death in a number of studies. GAL-3 was found to be up regulated in animal models of heart failure as well as myocardial infarction (MI). The objective of this study is to test if high GAL-3 after myocardial infarction has a protective role on the heart through its anti-apoptotic and anti-necrotic functions. Methods: Male C57B6/J mice and GAL-3 knockout (KO) mice were used for permanent ligation of the left anterior descending artery of the heart to create infarction in the anterior myocardium. Heart and plasma samples were collected 24 hours after the induction of MI and were used for immunohistochemistry, Tunnel procedure, electron microscopy and enzyme linked immunosorbent assay (ELISA). Results: Our results show that the significant increase in GAL-3 levels in the left ventricle at 24-hour following MI is associated with significant lower levels of pro-apoptotic proteins; cytochrome c, Bax, annexin V, cleaved caspase-3 and a higher levels of anti-apoptotic protein Bcl2 in GAL-3 wild MI group than GAL-3 KO group. We also have identified the anti-apoptotic activity of GAL-3 is mediated through a significant increase in Akt-1, NF kappa-B and beta-catenin proteins. In addition, we have identified the antiapoptotic activity is mediated through a significant lower levels of cathepsin-D protein. Conclusion: We conclude that the increased levels of GAL-3 at 24-hour following MI regulate antiapoptotic mechanisms in the myocardium that will shape the future course of the disease. We also identified that the anti-apoptotic mechanisms are likely mediated through interaction of GAL-3 with Akt-1, NF kappa-B, beta-catenin and cathepsin D proteins.

Original languageEnglish
Pages (from-to)287-302
Number of pages16
JournalCellular Physiology and Biochemistry
Volume54
Issue number2
DOIs
Publication statusPublished - 2020

Keywords

  • Apoptosis
  • Galectin 3
  • Heart
  • Myocardial infarction

ASJC Scopus subject areas

  • Physiology

Fingerprint

Dive into the research topics of 'Galectin-3: A cardiomyocyte antiapoptotic mediator at 24-hour post myocardial infarction'. Together they form a unique fingerprint.

Cite this