Aims
Galectin 3 (GAL-3) is a beta galactoside binding lectin that has different roles in normal and pathophysiological conditions. GAL-3 was found to be up regulated in animal models of myocardial infarction (MI). Cathepsins are intracellular lysosomal proteases that degrade proteins. The objective of his study is to investigate if high GAL-3 after myocardial infarction has a protective role on the heart through its modulation of lysosomal Cathepsins in ischemic myocardium.
Background/aims
Galectin 3 (GAL-3) is a beta galactoside binding lectin that has different roles in normal and pathophysiological conditions. GAL-3 was found to be up regulated in animal models of myocardial infarction (MI). Cathepsins are intracellular lysosomal proteases that degrade proteins. The objective of his study is to investigate if high GAL-3 after myocardial infarction has a protective role on the heart through its modulation of lysosomal Cathepsins in ischemic myocardium.
Conclusion
The increased levels of GAL-3 at 24-hour following MI regulates the process of cardiomyocytes injury through modulation of lysosomal cathepsins B, D, L and S.
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. Hearts and plasma samples were collected 24 hours after the induction of MI and were used for enzyme linked immunosorbent assay and immunofluorescent staining.
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 cathepsins B, D, L and S in GAL-3 wild MI group than GAL-3 KO MI group. We also report a significant lower plasma level of Troponin I in GAL-3 wild MI group than GAL-3 KO MI group.