Artículo de revista
Expression and function of toll-like receptor 4 and inflammasomes in cardiac fibroblasts and myofibroblasts: IL-1β synthesis, secretion, and degradation
Fecha
2016Registro en:
Molecular Immunology, Volumen 74,
18729142
01615890
10.1016/j.molimm.2016.05.001
Autor
Boza Fuentes, Pía
Ayala, Pedro
Vivar, Raúl
Humeres, Claudio
Cáceres, Felipe Tapia
Muñoz, Claudia
García Nannig, Lorena
Hermoso, Marcela A.
Díaz-Araya, Guillermo
Institución
Resumen
© 2016 Elsevier Ltd. Cardiac inflammation can be produced by pathogen-associated molecular patterns (PAMPs), from parasitic, bacterial or viral origin; or by danger-associated molecular patterns (DAMPs), released from dead cells after cardiac tissue damage, for example by cardiac infarction. Both, PAMPS and DAMPS activate TLR4 on resident immune cells and heart tissue cells, triggering an inflammatory process necessary to begin the wound healing process. Cardiac fibroblasts (CF) are the most abundant cells in the heart and are critical to wound healing, along with cardiac myofibroblasts (CMF), which are differentiated from CF through a TGF-β1-mediated process. While TLR4 and the inflammasome complex are known to play important roles in CF function, the effects of TGF-β1 on TLR4 and inflammasome expression and activity remain unknown. To elucidate this important point, we evaluated the effect of TGF-β1 on TLR4, and the inflammasome protein expression and activity through activation by L