کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5505333 | 1400265 | 2017 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Upregulated KAT7 in synovial fibroblasts promotes Th17Â cell differentiation and infiltration in rheumatoid arthritis
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Rheumatoid arthritis (RA) is a chronic autoimmune disease involving multiple cellular participants, of which synovial fibroblasts (SFs) are tightly connected with the development and progression of RA. Here, we provide evidence confirming that KAT7, an H4-specific histone acetylase, is upregulated in SFs of RA patients, which is at least attributed to the stimulation by RA-associated proinflammatory cytokines, such as TNF-α, IL-1β or IFN-γ. In addition, KAT7 overexpression in cultured human fibroblast-like synoviocytes (HFLSs) induces IL-6 and TGF-β expression through an epigenetic mechanism, and in vitro T helper 17 (Th17) cell polarization cultured in these supernatants shows promoted cell differentiation. Moreover, KAT7 overexpression in HFLSs induces CCL20 expression via p44/42 MAPK pathway, whereby promoting Th17 cell migration. These two activities of KAT7 in RA SFs indicate its potential roles in accelerating RA pathology. Overall, these results demonstrate some connections between KAT7 upregulated in RA SFs and RA progression and present the inhibition of KAT7 activity as a novel therapeutic target for interfering RA disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 489, Issue 2, 22 July 2017, Pages 235-241
Journal: Biochemical and Biophysical Research Communications - Volume 489, Issue 2, 22 July 2017, Pages 235-241
نویسندگان
Shouda Gao, Xiangbei Qi, Junke Li, Linchao Sang,