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Biomed Phys Eng Express ; 8(5)2022 07 07.
Artigo em Inglês | MEDLINE | ID: mdl-34243179

RESUMO

Cardiac arrhythmias represent about 50% of the cardiovascular diseases which are the first cause of mortality in the world. Implantable medical devices play a major role for treating these arrhythmias. Nevertheless the leads induce an unwanted biological phenomenon called fibrosis. This phenomenon begins at a cellular level and is effective at a macroscopic scale causing tissue remodelling with a local modification of the active cardiac tissue. Fibrosis mechanism is complex but at the cellular level, it mainly consists in cardiac fibroblasts activation and differentiation into myofibroblasts. We developed a simplifiedin vitromodel of cardiac fibrosis, with human cardiac fibroblasts whom differentiation into myofibroblasts was promoted with TGF-ß1. Our study addresses an unreported impedance-based method for real-time monitoring ofin vitrocardiac fibrosis. The objective was to study whether the differentiation of cardiac fibroblasts in myofibroblasts had a specific signature on the cell index, an impedance-based feature measured by the xCELLigence system. Primary human cardiac fibroblasts were cultured along 6 days, with or without laminin coating, to study the role of this adhesion protein in cultures long-term maintenance. The cultures were characterized in the presence or absence of TGF-ß1 and we obtained a significant cell index signature specific to the human cardiac fibroblasts differentiation.


Assuntos
Miofibroblastos , Fator de Crescimento Transformador beta1 , Células Cultivadas , Impedância Elétrica , Fibroblastos/metabolismo , Fibroblastos/patologia , Fibrose , Humanos , Miofibroblastos/metabolismo , Miofibroblastos/patologia , Fator de Crescimento Transformador beta1/metabolismo , Fator de Crescimento Transformador beta1/farmacologia
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