Effect of Galectin-3 Deficit on Ventricular Remodeling After Coronary Occlusion in Mice
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| Natura: | Artículo científico |
| Lingua: | en |
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Sociedad Argentina de Cardiología
2015
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| _version_ | 1876435607114219520 |
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| author | LUCIANA WILENSKY |
| author_facet | LUCIANA WILENSKY |
| contents | Effect of Galectin-3 Deficit on Ventricular Remodeling After Coronary Occlusion in Mice LUCIANA WILENSKY NADIA L. MARTÍNEZ NAYA PABLO CASSAGLIA VERÓNICA VOLBERG JULIA TAU EUGENIA ARUANNO ISAAC MORGUNOWSKY MICHELL CELINA MORALES Medicina Galectin Myocardial Infarction Ventricular Remodeling Background: Galectin-3 (Gal-3) is a lectin that regulates the immune response. However, its role in remodeling and ventricular function after myocardial infarction (MI) is unknown. Objective: The purpose of this study was to analyze whether Gal-3 deficit impairs remodeling and ventricular function after MI in mice. Methods: Male Gal-3KO mice and their respective C57 controls underwent anterior descending coronary artery ligation or sham operation. Animals were then divided into four experimental groups: 1) C57 sham; 2) Gal-3 KO sham; 3) C57 MI and 4) Gal-3 KO MI. Seven days after surgery, an echocardiography was performed followed by euthanasia. Heart samples were collected to measure MI size and fibrosis using Masson’s trichrome and picrosirius red, respectively, and assess macrophage infiltration and IL-6 expression. Results: Left ventricular diameters were significantly increased in the C57 MI group compared with sham animals and the increase was even higher in the Gal-3 KO MI group. Moreover, ejection fraction decreased to 47%±2% in C57 MI and 37%±3% in Gal-3 KO MI mice (p<0.02), and infarct size increased from 39.4%±5% in C57 MI to 66.8%±5% in Gal-3 KO MI animals (p=0.002). Macrophage infiltration and fibrosis in the MI area were significantly reduced in Gal-3 KO MI mice (p<0.001 C57MI vs. Gal-3KO MI) without changes of IL-6 concentration in the left ventricular free wall (p=ns). Conclusions: Gal-3 gene deletion is an important factor in repair kinetics, regulating macrophage infiltration and the degree of fibrosis in the infarct area, as well as early remodeling after MI. 2015 artículo científico 0034-7000 https://www.redalyc.org/articulo.oa?id=305341287005 en http://www.redalyc.org/revista.oa?id=3053 Revista Argentina de Cardiología application/pdf Sociedad Argentina de Cardiología Revista Argentina de Cardiología (Argentina) Num.4 Vol.83 |
| format | Artículo científico |
| id | redalyc_305341287005 |
| institution | Redalyc |
| language | en |
| publishDate | 2015 |
| publisher | Sociedad Argentina de Cardiología |
| spellingShingle | Effect of Galectin-3 Deficit on Ventricular Remodeling After Coronary Occlusion in Mice LUCIANA WILENSKY Medicina Galectin Myocardial Infarction Ventricular Remodeling Effect of Galectin-3 Deficit on Ventricular Remodeling After Coronary Occlusion in Mice LUCIANA WILENSKY NADIA L. MARTÍNEZ NAYA PABLO CASSAGLIA VERÓNICA VOLBERG JULIA TAU EUGENIA ARUANNO ISAAC MORGUNOWSKY MICHELL CELINA MORALES Medicina Galectin Myocardial Infarction Ventricular Remodeling Background: Galectin-3 (Gal-3) is a lectin that regulates the immune response. However, its role in remodeling and ventricular function after myocardial infarction (MI) is unknown. Objective: The purpose of this study was to analyze whether Gal-3 deficit impairs remodeling and ventricular function after MI in mice. Methods: Male Gal-3KO mice and their respective C57 controls underwent anterior descending coronary artery ligation or sham operation. Animals were then divided into four experimental groups: 1) C57 sham; 2) Gal-3 KO sham; 3) C57 MI and 4) Gal-3 KO MI. Seven days after surgery, an echocardiography was performed followed by euthanasia. Heart samples were collected to measure MI size and fibrosis using Masson’s trichrome and picrosirius red, respectively, and assess macrophage infiltration and IL-6 expression. Results: Left ventricular diameters were significantly increased in the C57 MI group compared with sham animals and the increase was even higher in the Gal-3 KO MI group. Moreover, ejection fraction decreased to 47%±2% in C57 MI and 37%±3% in Gal-3 KO MI mice (p<0.02), and infarct size increased from 39.4%±5% in C57 MI to 66.8%±5% in Gal-3 KO MI animals (p=0.002). Macrophage infiltration and fibrosis in the MI area were significantly reduced in Gal-3 KO MI mice (p<0.001 C57MI vs. Gal-3KO MI) without changes of IL-6 concentration in the left ventricular free wall (p=ns). Conclusions: Gal-3 gene deletion is an important factor in repair kinetics, regulating macrophage infiltration and the degree of fibrosis in the infarct area, as well as early remodeling after MI. 2015 artículo científico 0034-7000 https://www.redalyc.org/articulo.oa?id=305341287005 en http://www.redalyc.org/revista.oa?id=3053 Revista Argentina de Cardiología application/pdf Sociedad Argentina de Cardiología Revista Argentina de Cardiología (Argentina) Num.4 Vol.83 |
| title | Effect of Galectin-3 Deficit on Ventricular Remodeling After Coronary Occlusion in Mice |
| topic | Medicina Galectin Myocardial Infarction Ventricular Remodeling |
| url | https://www.redalyc.org/articulo.oa?id=305341287005 |