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Heart Lung Circ. 2017 Jul;26(7):736-745. doi: 10.1016/j.hlc.2016.11.007. Epub 2016 Dec 19.

Myocardial and Serum Galectin-3 Expression Dynamics Marks Post-Myocardial Infarction Cardiac Remodelling.

Author information

1
Division of Cardiovascular Medicine, University at Buffalo, Buffalo, NY, USA. Electronic address: sharmau@buffalo.edu.
2
Division of Cardiovascular Medicine, University at Buffalo, Buffalo, NY, USA.
3
Department of Bioinformatics-BiGCaT, University of Maastricht, Maastricht, The Netherlands.
4
Department of Pathology and Oncology, Roswell Park Cancer Institute, Buffalo, NY, USA.
5
Department of Pharmacology, University of Maastricht, Maastricht, The Netherlands.

Abstract

BACKGROUND:

Acute myocardial infarction (MI) causes significant changes in cardiac morphology and function. Galectin-3 is a novel and potentially therapeutically important mediator of cardiac remodelling. Myocardial and serum galectin-3 expression dynamics in response to the early cardiovascular outcomes after acute MI are not fully elucidated.

METHODS:

We first performed a comprehensive longitudinal microarray analyses in mice after acute MI. We then measured the serum levels of galectin-3 in a translational porcine model of coronary microembolism-induced post-ischaemic cardiac remodelling. We validated our pre-clinical studies in humans by measuring serum galectin-3 levels of 52 patients with acute ST-elevation MI (STEMI) and 11 healthy controls. We analysed galectin-3 data in relation to the development of major adverse cardiovascular outcomes (MACO).

RESULTS:

Of the 9,753 genes profiled at infarcted and remote myocardium at eight different time points, dynamic myocardial overexpression of galectin-3 mRNA was detected. In a pig model of diffuse myocardial damage and cardiac remodelling, galectin-3 localised to the areas of tissue damage and myocardial fibrosis, with proportionate increase of their serum galectin-3 expression levels. In humans, increased serum galectin-3 level was associated with in-hospital MACO.

CONCLUSIONS:

In this translational study, we demonstrated that galectin-3 is dynamically overexpressed in response to acute MI-induced cardiac remodelling. Elevated galectin-3 levels are associated with the development of in-hospital MACO.

KEYWORDS:

Fibrosis; Galectin-3; Microarrays; Myocardial infarction; Remodelling

PMID:
28094123
PMCID:
PMC5459666
DOI:
10.1016/j.hlc.2016.11.007
[Indexed for MEDLINE]
Free PMC Article

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