کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8258659 | 1534611 | 2018 | 35 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
miR-146a regulates inflammatory cytokine production in Porphyromonas gingivalis lipopolysaccharide-stimulated B cells by targeting IRAK1 but not TRAF6
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کلمات کلیدی
PBSLPSmiRsP. gingivalisGAPDHA. actinomycetemcomitansAggregatibacter actinomycetemcomitansIRAK1TRAF6interleukin - اینترلوکینmiR-146a - به miR-146AELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاmicroRNAs - ریز آرانایTNF receptor associated factor 6 - فاکتور مرتبط با گیرنده TNF 6phosphate buffer saline - فسفات بافر شورB cell - لنفوسیت بیlipopolysaccharide - لیپوپلی ساکاریدUTR یا untranslated regions - منطقه ترجمه نشدهuntranslated region - منطقه غیر ترجمهoptical density - چگالی نوریPorphyromonas gingivalis - ژنژیوالیس پورفیروموناسglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
It has been suggested that microRNAs (miRs) are involved in the immune regulation of periodontitis. However, it is unclear whether and how miRs regulate the function of B cells in the context of periodontitis. This study is to explore the role of miR-146a on the inflammatory cytokine production of B cells challenged by Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS). Primary B cells were harvested from mouse spleen. Quantitative real-time polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA) were used to detect the expression of inflammatory cytokines in B cells in the presence or absence of P. gingivalis LPS and/or miR-146a. Bioinformatics, luciferase reporter assay and overexpression assay were used to explore the binding target of miR-146a. Our results showed that miR-146a level in B cells was elevated by P. gingivalis LPS stimulation, and the mRNA expressions of interleukin (IL)-1β, 6 and 10, and IL-1 receptor associated kinase-1 (IRAK1), but not TNF receptor associated factor 6 (TRAF6), were also upregulated. The expression levels of IL-1β, 6, 10 and IRAK1 were reduced in the presence of miR-146a mimic, but were elevated by the addition of miR-146a inhibitor. MiR-146a could bind with IRAK1 3â² untranslated region (UTR) but not TRAF6 3â²-UTR. Overexpression of IRAK1 reversed the inhibitory effects of miR-146a on IL-1β, 6 and 10. In summary, miR-146a inhibits inflammatory cytokine production in B cells through directly targeting IRAK1, suggesting a regulatory role of miR-146a in B cell-mediated periodontal inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1864, Issue 3, March 2018, Pages 925-933
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1864, Issue 3, March 2018, Pages 925-933
نویسندگان
Shaoyun Jiang, Yang Hu, Shu Deng, Jiayin Deng, Xinbo Yu, Grace Huang, Toshihisa Kawai, Xiaozhe Han,