Abstract 412: Galectin-3 Promotes Pro-Hypertrophic Communication Between Fibroblasts and Cardiomyocytes
| Autor: | Mario Bustamante, Ingrid Oyarzun, Georthan Mancilla, Clara Quiroga, Hugo E Verdejo, Pablo Castro |
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| Rok vydání: | 2017 |
| Předmět: | |
| Zdroj: | Circulation Research. 121 |
| ISSN: | 1524-4571 0009-7330 |
| Popis: | Galectin-3 (gal-3) is a β-galactoside-binding protein used as a prognostic biomarker in chronic heart failure (CHF) patients. Genetic and pharmacologic studies show that gal-3 is required for cardiac remodeling in animal models of CHF, suggesting an active role for gal-3 in the progression of the disease, but the mechanism involved is largely unknown. We assessed the hypothesis that gal-3 induces cardiac remodeling, causing both cardiomyocyte hypertrophy and fibroblasts activation through a mechanism involving intercellular communication. As a model, we used neonatal rat ventricular cardiomyocytes (NRVM), and fibroblasts (NRVF) stimulated with recombinant gal-3. We assessed cell death and proliferation by flow cytometry and MTT assays. To elucidate the signaling pathways involved, we quantified relative changes in protein levels by Western blot. To determine cell size and sarcomerization, we used confocal microscopy. Changes in mRNA and microRNA expression were analyzed by qPCR. Our results show that gal-3 does not induce hypertrophy or sarcomerization on isolated NRVM culture. On the other hand, NRVF treated with gal-3 exhibit an increase in ERK1/2 (n=3, p |
| Databáze: | OpenAIRE |
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