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ER Stress-induced Inflammasome Activation Contributes to Hepatic Inflammation and Steatosis.
Zhang, Jinyu; Zhang, Kezhong; Li, Zihai; Guo, Beichu.
Afiliación
  • Zhang J; Department of Microbiology and Immunology, Medical University of South Carolina (MUSC), Charleston, South Carolina 29425-5040, USA; Hollings Cancer Center, Medical University of South Carolina (MUSC), Charleston, South Carolina 29425, USA.
  • Zhang K; Department of Immunology and Microbiology, Center for Molecular Medicine & Genetics, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI 48201, USA.
  • Li Z; Department of Microbiology and Immunology, Medical University of South Carolina (MUSC), Charleston, South Carolina 29425-5040, USA; Hollings Cancer Center, Medical University of South Carolina (MUSC), Charleston, South Carolina 29425, USA.
  • Guo B; Department of Microbiology and Immunology, Medical University of South Carolina (MUSC), Charleston, South Carolina 29425-5040, USA; Hollings Cancer Center, Medical University of South Carolina (MUSC), Charleston, South Carolina 29425, USA.
J Clin Cell Immunol ; 7(5)2016 Oct.
Article en En | MEDLINE | ID: mdl-27942420
ABSTRACT
Endoplasmic reticulum (ER) stress functions as a protein folding and quality control mechanism to maintain cell homeostasis. Emerging evidence indicates that ER stress is also involved in metabolic and inflammatory diseases. However, the link between ER stress and inflammation remains not well characterized. In this study, we have demonstrated that ER stress-induced inflammasome activation plays a critical role in the pathogenesis of hepatic steatosis. By utilizing genetic and pharmacological agent-induced hepatic steatosis animal models, we found that hepatic steatosis was associated with inflammasome activation and ER stress. Our results show that caspase-1 ablation alleviated liver inflammation and injury. Liver tissues from caspase-1 KO mice had significantly reduced production of IL-1ß under ER stress conditions. We also found that ER stress promoted inflammasome activation and IL-1ß processing in both hepatocytes and Kupffer cells/macrophages. Moreover, lack of caspase-1 ameliorated cell death or pyropoptosis of hepatocytes induced by ER stress. Taken together, our findings suggest that ER stress-induced inflammasome activation and IL-1ß production generate a positive feedback loop to amplify inflammatory response, eventually leading to liver steatosis and injury.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: J Clin Cell Immunol Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: J Clin Cell Immunol Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos