Endoplasmic reticulum stress induced by lipopolysaccharide is involved in the association between inflammation and autophagy in INS1 cells.
Mol Med Rep
; 16(5): 5787-5792, 2017 Nov.
Article
em En
| MEDLINE
| ID: mdl-28849211
ABSTRACT
Type 2 diabetes is a chronic inflammatory disease. Autophagy, the dynamic process of lysosomal degradation of damaged organelles and proteins, may protect ßcells from destruction by inflammation in type 2 diabetes. The present study investigated the role of autophagy, inflammation and endoplasmic reticulum (ER) stress in type 2 diabetes. INS1 cells were incubated with lipopolysaccharide. The chemical chaperone 4phenylbutyric acid was used to inhibit ER stress, and 3methyadenine (3MA) was used to inhibit autophagy. Apoptosis was detected by flow cytometry and cell proliferation using Cell Counting kit8 solution. Light chain3B, interleukin (IL) 1ß, caspase1 and C/EBP homologous protein production were assessed by western blotting, and rat activating transcription factor 4 and rat binding immunoglobulin heavy chain protein gene expression were determined by realtime reverse transcriptionpolymerase chain reaction. The results showed that inhibiting autophagy with 3MA unexpectedly contributed to cell death in ßcells. This response was associated with an increase in inflammatory cytokines, including IL1ß and caspase1. Inhibiting ER stress with 4phenylbutyric acid led to a decrease in cell apoptosis. These results showed that autophagy may have a protective effect by reducing inflammatory cytokines in ßcells. In addition, the inositolrequiring enzyme 1 pathway mediated the ER stress associated with autophagy and inflammatory cytokines (IL1ß and caspase1). Therefore, inflammatory cytokines may be critical signalling nodes, which are associated with ER stressmediated ßcell death.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Diabetes Mellitus Tipo 2
/
Estresse do Retículo Endoplasmático
/
Inflamação
Tipo de estudo:
Risk_factors_studies
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Mol Med Rep
Ano de publicação:
2017
Tipo de documento:
Article