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Role of Endoplasmic Reticulum Stress in Rheumatoid Arthritis Pathogenesis
Journal of Korean Medical Science ; : 2-11, 2014.
Article in English | WPRIM | ID: wpr-53763
ABSTRACT
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by abnormal proliferation of synoviocytes, leukocyte infiltration, and angiogenesis. The endoplasmic reticulum (ER) is the site of biosynthesis for all secreted and membrane proteins. The accumulation of unfolded proteins in the ER leads to a condition known as ER stress. Failure of the ER's adaptive capacity results in abnormal activation of the unfolded protein response. Recently, we have demonstrated that ER stress-associated gene signatures are highly expressed in RA synovium and synovial cells. Mice with Grp78 haploinsufficiency exhibit the suppression of experimentally induced arthritis, suggesting that the ER chaperone GRP78 is crucial for RA pathogenesis. Moreover, increasing evidence has suggested that GRP78 participates in antibody generation, T cell proliferation, and pro-inflammatory cytokine production, and is therefore one of the potential therapeutic targets for RA. In this review, we discuss the putative, pathophysiological roles of ER stress and GRP78 in RA pathogenesis.
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Full text: Available Index: WPRIM (Western Pacific) Main subject: Arthritis, Rheumatoid / Autoantibodies / Synovial Membrane / Lymphocyte Activation / T-Lymphocytes / Cytokines / Protein Folding / Cell Proliferation / Endoplasmic Reticulum / Unfolded Protein Response Type of study: Etiology study Limits: Animals / Humans Language: English Journal: Journal of Korean Medical Science Year: 2014 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Arthritis, Rheumatoid / Autoantibodies / Synovial Membrane / Lymphocyte Activation / T-Lymphocytes / Cytokines / Protein Folding / Cell Proliferation / Endoplasmic Reticulum / Unfolded Protein Response Type of study: Etiology study Limits: Animals / Humans Language: English Journal: Journal of Korean Medical Science Year: 2014 Type: Article