IBIOBA - MPSP 22718
INSTITUTO DE INVESTIGACION EN BIOMEDICINA DE BUENOS AIRES - INSTITUTO PARTNER DE LA SOCIEDAD MAX PLANCK
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Cytokine-induced endoplasmic reticulum stress in beta-cells is ameliorated by Compound A
Autor/es:
GIMENO, MARÍA LAURA; ANDREONE, LUZ; ARIOLFO, LAURA; BARCALA TABARROZZI, ANDRES E; FUERTES, FLORENCIA; DE BOSSCHER, KAROLIEN; GERLO, SARAH; LIBERMAN, ANA C; PERONE, MARCELO JAVIER
Lugar:
Buenos Aires
Reunión:
Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017
Institución organizadora:
SAIC - Trabajo seleccionado para competir por Premio Gador
Resumen:
Type 1 diabetes (T1D) is a T cell-mediated autoimmune disease that selectively destroys insulin producing β-cells. ER stress and subsequent insulin secretory deficiency in β-cells precede the onset of autoimmune diabetes. Pro-inflammatory cytokines (IL-1+IFN-; CYT) signaling leads to activation of ER stress in β-cells. We reported that Compound A (2-(4-acetoxyphenyl)-2-chloro-N-methyl-ethylammonium chloride; CpdA), a dissociative glucocorticoid receptor (GR)-ligand, is an effective modulator of T and dendritic cells. The aim of this study was to explore the beneficial effects of CpdA on CYT-induced β-cell ER stress; the classic GR-ligand dexamethasone was used for comparison. CpdA significantly reduced CYT-induced NO secretion by the insulinoma INS-1E cells (p
