Galectin-1 in early acute myocardial infarction

• Published in: PloS one 2014-01, Vol.9 (1), p.e86994-e86994
• Main Authors: Al-Salam, Suhail, Hashmi, Satwat
• Format: Article
• Language: English
• Subjects: Analysis; Animals; Apoptosis; Biology; Cardiovascular disease; Cell cycle; Complications; Coronary artery; Coronary artery disease; Enzyme-Linked Immunosorbent Assay; Fluorescent Antibody Technique; Galectin 1 - blood; Galectin 1 - metabolism; Galectin-1; Health aspects; Health sciences; Heart; Heart attack; Heart attacks; Heart diseases; Hypoxia; Hypoxia-inducible factor 1; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism; Immunohistochemistry; Ischemia; Kinases; Laboratory animals; Male; Mammals; Medicine; Mice; Mice, Inbred C57BL; Morbidity; Myocardial infarction; Myocardial Infarction - blood; Myocardial Infarction - metabolism; Myocardial ischemia; Myocardium - metabolism; Myocardium - pathology; Pathology; Proteins; Proto-Oncogene Proteins c-bcl-2 - metabolism; Rodents; Stem cells; Studies; Time Factors; Ventricle
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0086994

Myocardial infarction (MI) is the most serious manifestation of coronary artery disease and the cause of significant mortality and morbidity worldwide. Galectin-1(GAL-1), a divalent 14.5-kDa protein, is present both inside and outside cells, and has both intracellular and extracellular functions. Hypoxia inducible factor-1 alpha (HIF-1α) is a transcription factor mediating early and late responses to myocardial ischemia. Identification of the pattern of expression of GAL-1 and HIF-1α in the heart during the first 24 hours following acute MI will help in understanding early molecular changes in this event and may provide methods to overcome serious complications. Mouse model of MI was used and heart samples were processed for immunohistochemical and immunofluorescent labeling and Enzyme linked immunosorbent assay to identify GAL-1 and HIF 1α levels in the heart during the first 24 hours following MI. There was significant increase in left ventricular GAL-1 at 20 (p = 0.001) and 30 minutes (p = 0.004) following MI. There was also a significant increase in plasma GAL-1 at 4 hours (p = 0.012) and 24 hours (p = 0.001) following MI. A significant increase in left ventricular HIF-1 α was seen at 20 minutes (p = 0.047) following MI. In conclusion, we show for the first time that GAL-1 level in the left ventricle is increased in early ischemic period. We also report for the first time that HIF-1 α is significantly increased at 20 minutes following MI. In addition we report for the first time that mouse plasma GAL-1 level is significantly raised as early as 4 hours following MI.