Artículo de revista
Pro-inflammatory cytokines enhance ERAD and ATF6α pathway activity in salivary glands of Sjögren's syndrome patients
Fecha
2016Registro en:
Journal of Autoimmunity, Volumen 75,
10959157
08968411
10.1016/j.jaut.2016.07.006
Autor
Barrera, María José
Aguilera, Sergio
Castro, Isabel
Cortés Araya, Juan Eliecer
Bahamondes, Verónica
Quest, Andrew F. G.
Molina, Claudio
González, Sergio
Hermoso Ramello, Marcela
Urzúa, Ulises
Leyton Campos, Lisette
González Burgos, María Julieta
Institución
Resumen
© 2016 Elsevier Ltd Salivary gland (SG) acinar-cells are susceptible to endoplasmic reticulum (ER) stress related to their secretory activity and the complexity of synthesized secretory products. SGs of Sjögren's syndrome patients (SS)-patients show signs of inflammation and altered proteostasis, associated with low IRE1α/XBP-1 pathway activity without avert increases in apoptosis. Acinar-cells may avoid apoptosis by activation of the ATF6α pathway and ER-associated protein degradation (ERAD). The aim of this study was to evaluate the role of pro-inflammatory cytokines in ATF6α pathway/ERAD activation and cell viability in labial salivary glands (LSG) of SS-patients. In biopsies from SS-patients increased ATF6α signaling pathway activity, as evidenced by generation of the ATF6f cleavage fragment, and increased expression of ERAD machinery components, such as EDEM1, p97, SEL1L, gp78, UBE2J1, UBE2G2, HERP and DERLIN1, were observed compared to controls. Alternatively, for pro- (active-ca