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The Role of Toll‐Like Receptor 4 in the Development of Cardiomyocyte Hypertrophy in vitro: Participation of NF‐κB Signalling
Author(s) -
Alvim Juliana Morais,
Silva Fernanda Gaisler,
CarneiroRamos Marcela Sorelli
Publication year - 2016
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.30.1_supplement.lb573
Subject(s) - tlr4 , agonist , innate immune system , toll like receptor , muscle hypertrophy , receptor , in vitro , microbiology and biotechnology , gq alpha subunit , biology , signal transduction , medicine , endocrinology , immunology , g protein , biochemistry
Objectives Toll like receptors (TLR), which plays an important role in innate immunity, inflammatory process and infection, activates the NF‐kB pathway and regulates inflammatory cytokines expression. Some systemic or local inflammations are followed by cardiovascular diseases, showing that this cytokines are responsible for modulating the cardiac tropism, decreasing the cardiac contractile. Studies using isolated cardiomyocytes allow a specific evaluation of the effects caused by the hypertrophic stimuli as well as the characterization of signalling pathway involved in this process. The aim of this study is to evaluate the role of Nf‐kB signaling in cardiomyocyte tropism after TLR activation. Methods Cardiomyocytes were isolated from wistar neonatal rats (in accordance with the ethical committee), presenting typical morphological and contractile characteristics that were maintained through the entire experiment. Cells were treated for 24hs with five different concentrations of LPS (TLR4 agonist) in order to define the dose that induces greater hypertrophic response. ANF and Alpha‐actin mRNA levels were used as cardiac hypertrophy markers. Gene expression was evaluated by Real‐time PCR. The results were expressed as mean ±SD and P<0.05. Results Alpha‐actin mRNA levels has increased approximately 50% after 100uM of LPS treatment compared with control group (p<0.05). Conclusion These results suggest that TLR4 was activated by their agonist and promoted cardiomyocytes hypertrophy in vitro. Support or Funding Information Financial support given by FAPESP, CAPES and UFABC.