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BioMed Research International
Volume 2016, Article ID 2634976, 7 pages
http://dx.doi.org/10.1155/2016/2634976
Research Article

Role of Histone Demethylases in Cardiomyocytes Induced to Hypertrophy

1Center of Biomedical Research Universidad de La Sabana (CIBUS), Chía, Colombia
2Fundación Cardioinfantil, Instituto de Cardiología, Bogotá, Colombia

Received 3 May 2016; Revised 17 August 2016; Accepted 22 August 2016

Academic Editor: Wen-Hwa Lee

Copyright © 2016 Wendy Rosales et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Epigenetic changes induced by histone demethylases play an important role in differentiation and pathological changes in cardiac cells. However, the role of the jumonji family of demethylases in the development of cardiac hypertrophy remains elusive. In this study, the presence of different histone demethylases in cardiac cells was evaluated after hypertrophy was induced with neurohormones. A cell line from rat cardiomyocytes was used as a biological model. The phenotypic profiles of the cells, as well as the expression of histone demethylases, were studied through immunofluorescence, transient transfection, western blot, and qRT-PCR analysis after inducing hypertrophy by angiotensin II and endothelin-1. An increase in fetal gene expression (ANP, BNP, and β-MHC) was observed in cardiomyocytes after treatment with angiotensin II and endothelin-1. A significant increase in JMJD2A expression, but not in UTX or JMJD2C expression, was observed. When JMJD2A was overexpressed in cardiomyocytes through transient transfection, the effect of neurohormones on fetal cardiac gene expression was increased. We conclude that JMJD2A plays a principal role in the regulation of fetal cardiac genes, which increase in expression during the pathological hypertrophic process.