دورية أكاديمية
Small heterodimer partner interacting leucine zipper protein (SMILE) ameliorates autoimmune arthritis via AMPK signaling pathway and the regulation of B cell activation
العنوان: | Small heterodimer partner interacting leucine zipper protein (SMILE) ameliorates autoimmune arthritis via AMPK signaling pathway and the regulation of B cell activation |
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المؤلفون: | JooYeon Jhun, Jeonghyeon Moon, Ji Ye Kwon, Keun-Hyung Cho, Seang Yoon Lee, Hyun Sik Na, Mi-La Cho, Jun-Ki Min |
المصدر: | Cell Communication and Signaling, Vol 21, Iss 1, Pp 1-14 (2023) |
بيانات النشر: | BMC, 2023. |
سنة النشر: | 2023 |
المجموعة: | LCC:Medicine LCC:Cytology |
مصطلحات موضوعية: | Small heterodimer partner-interacting leucine zipper protein (SMILE), Rheumatoid arthritis (RA), B cell, BAFF receptor, AMPK/mTOR, Medicine, Cytology, QH573-671 |
الوصف: | Abstract Rheumatoid arthritis (RA) is an autoimmune disease that causes joint swelling and inflammation and can involve the entire body. RA is characterized by the increase of pro-inflammatory cytokines such as interleukin (IL) and tumor necrosis factor, and the over-activation of T lymphocytes and B lymphocytes, which may lead to severe chronic inflammation of joints. However, despite numerous studies the pathogenesis and treatment of RA remain unresolved. This study investigated the use of small heterodimer partner-interacting leucine zipper protein (SMILE) overexpression to treat a mouse model of RA. SMILE is an insulin-inducible corepressor through adenosine monophosphate-activated kinase (AMPK) signaling pathway. The injection of a SMILE overexpression vector to mice with collagen induced-arthritis resulted in a milder clinical pathology and a reduced incidence of arthritis, less joint tissue damage, and lower levels of Th17 cells and plasma B cells in the spleen. Immunohistochemistry of the joint tissue showed that SMILE decreased B-cell activating factor (BAFF) receptor (BAFF-R), mTOR, and STAT3 expression but increased AMPK expression. In SMILE-overexpressing transgenic mice with collagen antibody-induced arthritis (CAIA), a decrease in the arthritis score and reductions in tissue damage, the number of B cells, and antibody production were observed. The treatment of immune cells in vitro with curcumin, a known SMILE-inducing agent, led to decreases in plasma B cells, germinal center B cells, IL-17-producing B cells, and BAFF-R-positive B cells. Taken together, our findings demonstrate the therapeutic potential of SMILE in RA, based on its inhibition of B cell activation mediated by the AMPK/mTOR and STAT3 signaling pathway and BAFF-R expression. Video abstract |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1478-811X |
Relation: | https://doaj.org/toc/1478-811X |
DOI: | 10.1186/s12964-023-01054-y |
URL الوصول: | https://doaj.org/article/173ad8f7b5f74ca58e9e284765cac4db |
رقم الأكسشن: | edsdoj.173ad8f7b5f74ca58e9e284765cac4db |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 1478811X |
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DOI: | 10.1186/s12964-023-01054-y |