期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 182, 期 1, 页码 29-40出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2012.09.022
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资金
- American Heart Association Scientist development grant (national)
- Argentinean National Agency for Promotion of Science and Technology, University of Buenos Aires
- Fundacion Sales
- NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [KL2TR000057] Funding Source: NIH RePORTER
Galectin-1 (Gal-1), an evolutionarily conserved beta-galactoside-binding lectin, plays essential roles in the control of inflammation and neovascularization. Although identified as a major component of the contractile apparatus of cardiomyocytes, the potential role of Gal-1 in modulating heart pathophysiology is uncertain. Here, we aimed to characterize Gal-1 expression and function in the infarcted heart. Expression of Gal-1 was substantially increased in the mouse heart 7 days after acute myocardial infarction (AMI) and in hearts from patients with end-stage chronic heart failure. This lectin was localized mainly in cardiomyocytes and inflammatory infiltrates in pen-infarct areas, but not in remote areas. Both simulated hypoxia and proinflammatory cytokines selectively up-regulated Gal-1 expression in mouse cardiomyocytes, whereas anti-inflammatory cytokines inhibited expression of this Lectin or had no considerable effect. Compared with their wild-type counterpart, Gal-1-deficient (Lgals1(-/-)) mice showed enhanced cardiac inflammation, characterized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced frequency of regulatory I cells, Leading to impaired cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI. Treatment of mice with recombinant Gal-1 attenuated cardiac damage in reperfused AMI. Taken together, our results indicate a protective role for Gal-1 in normal cardiac homeostasis and post-infarction remodeling by preventing cardiac inflammation. Thus, Gal-1 treatment represents a potential novel strategy to attenuate heart failure in AMI. (Am J Pathol 2013, 182: 29-40; http://dx.doi.org/10.1016/j.ajpath.2012.09.022)
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