Premium
Thyroid hormone influences calgranulin A and B expression in heart and cardiac myocytes cells
Author(s) -
Takano Ana Paula Cremasco,
Moriscot Anselmo Sigari,
BarretoChaves Maria Luiza Morais
Publication year - 2013
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.27.1_supplement.1197.7
Subject(s) - proinflammatory cytokine , stimulation , context (archaeology) , western blot , messenger rna , medicine , endocrinology , myocyte , gene expression , tlr4 , biology , chemistry , gene , receptor , inflammation , biochemistry , paleontology
Previous findings of our group showed a global set of responsive genes to triiodotyronine (T3) in the heart including proinflammatory genes. In this context, calgranulin A and B (S100A8 and S100A9 respectively) are proteins associated with decreased contractility and considered important molecules that are able to bind to TLR4 and consequently initiate signaling pathways with fundamental role during inflammatory process. mRNA expression of calgranulin A and B in the heart of rats treated with T3 (7 μg/100g of body weight/day) for 24 h, 7 and 14 days and also in rats neonatal cardiomyocytes stimulated with T3 (10 nM) for 24 h was analyzed by Real Time PCR. TLR4 protein expression was also evaluated by western blot. Data were presented as mean±SD and t test or one‐way analysis of variance was used. P <0.05 values were considered statistically significant. T3 stimulation induced a significant up‐regulation of calgranulin A and B in hearts (2 fold) starting at 24h up to 7 and 14 days and also in isolated cardiomyocytes cells. The TLR4 protein expression was not altered after T3 treatment. The increased calgranulins mRNA levels point to a possible role of proinflammatory genes on cardiac or cardiomyocytic hypertrophy process induced by T3 and additional experiments are being conducted to better answer this question.