A selective glucocorticoid receptor modulator (CpdA) attenuates cytokine-induced endoplasmic reticulum stress in β-cells.

BARCALA TABARROZZI, ANDRES E; LIBERMAN, ANA C; PERONE, MARCELO JAVIER; GIMENO, MARÍA LAURA; ELÍAS, MARIANA JUDITH; DE BOSSCHER, KAROLIEN; ANDREONE, LUZ; ARIOLFO, LAURA; GERLO, SARAH

Buenos Aires

Congreso; The 21st International Association of Pancreatology (IAP)/LAPSG Joint Meeting, Pancreas 2017; 2017

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-1b+IFN-g; 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 cytokine-induced β-cell ER stress. CpdA significantly reduced CYT-induced NO secretion by INS-1E cells (p