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AMPK signaling pathway is downregulated by Thyroid Hormone in cardiomyocytes
Author(s) -
Takano Ana Paula Cremasco,
Diniz Gabriela Placoná,
Chaves Maria Luiza Morais Barreto
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.622.5
Subject(s) - ampk , endocrinology , signal transduction , medicine , protein kinase a , hormone , western blot , phosphorylation , thyroid , muscle hypertrophy , chemistry , kinase , biology , microbiology and biotechnology , biochemistry , gene
Objective Thyroid hormone (TH) modulates rapidly several signaling pathways which have been implicated in cardiac hypertrophy. In addition, the AMP‐activated protein kinase (AMPK) also plays an important role in regulating cardiac hypertrophy. The aim of the present study was to investigate the TH effect on AMPK signaling pathway in cardiomyocytes. Methods Cardiomyocytes cultures were prepared from ventricles of neonatal Wistar rats by colagenase/pancreatin method. The cells were treated with serum‐free medium (control cells) or serum‐free medium containing T3 (10nM) for 5, 10, 15 and 30 minutes. The AMPK, LKB1 and protein phosphatase 2C (PP2C) were analyzed by Western Blot. Data were presented as mean±SD and were evaluated using one‐way analysis of variance. Values of P<0.05 were considered statistically significant. Results The cardiomyocytes treated with T3 for 10 and 15 minutes presented a significant decrease on AMPK (86.21±4.62 and 74.32±9.23, P<0.05) and LKB1 (65.18±5.17 and 67.43±4.92, P<0.01) phosphorylation levels, as well as on PP2C levels (77.5±5.55 and 75.21±9.83, P<0.05) in relation to control cells. Conclusion These data demonstrate for the first time that TH modulates rapidly the AMPK signaling pathway in cardiomyocytes cultures. The possible involvement of this signaling pathway in the modulation of TH‐induced cardiomyocyte hypertrophy remains to be investigated.