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NF‐қB Activation is Required for Thyroid Hormone Induced Cardiomyocyte Hypertrophy
Author(s) -
Takano Ana Paula,
Moriscot Anselmo,
BarretoChaves Maria Luiza
Publication year - 2015
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.29.1_supplement.1043.2
Subject(s) - nf κb , muscle hypertrophy , endocrinology , medicine , western blot , nfkb1 , iκbα , hormone , gene expression , signal transduction , blot , transcription factor , biology , chemistry , gene , microbiology and biotechnology , inflammation , biochemistry
The nuclear factor NF‐қB promotes inflammatory response and mediates cardiac growth by different hypertrophic stimuli. We have previous results obtained by microarray experiments indicating that thyroid hormone (triiodotyronine, T3) up‐regulates pro‐inflammatory genes. Considering that, we investigated the influence of T3 on NF‐қB signaling and the possible participation of this nuclear factor in cardiomyocyte hypertrophy induced by T3. Primary cultures of neonatal rat ventricular cardiomyocytes were treated with T3 for 10, 30 minutes and 24 hours and the NF‐қB signaling was analyzed by western blot. Also, cardiomyocytes were treated with an inhibitor of NF‐қB (JSH‐23) followed by treatment with T3 for evaluation of mRNA expression of atrial natriuretic factor (ANF) and cell surface area analysis. Data were presented as mean ± SD and were analyzed using one‐way ANOVA and Tukey multiple comparisons test. Values of p<0.05 were considered statistically significant. T3 rapidly increased the nuclear protein expression of NF‐қB without alterations on IKK and IқB expression. The inhibition of NF‐қB reduced both ANF mRNA levels and the surface area of cardiomyocytes compared to T3 treated cells. These results confirm that NF‐қB is required for development of cardiomyocyte hypertrophy by T3. The possible interactions of NF‐қB with genes associated with cardiac growth are being investigated. Financial support: Fapesp (2013/22480‐4 and 2011/23352‐4).

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