کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
11030718 | 1646183 | 2018 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
microRNA-199a may be involved in the pathogenesis of lupus nephritis via modulating the activation of NF-κB by targeting Klotho
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
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چکیده انگلیسی
Klotho is considered to have renal protective effect by prohibiting the activation of the nuclear factor (NF)-κB pathway, while the role of microRNA-199a (miR-199a)/Klotho in lupus nephritis (LN) is still unknown. A single dose of pristane (0.5âml) was intraperitoneally injected into 8 weeks-old female mice to establish the LN model. MiR-199a mimic or miR-199a inhibitor, Klotho plasmid or Klotho siRNA, and miR-199a inhibitor plus si-Klotho were transfected into lipopolysaccharides (LPS) stimulated human embryonic kidney 293âT (HEK293âT) cells. Western Blot was adopted to measure p-P65 expression. Tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the supernatant were determined by enzyme-linked immunosorbent assay (ELISA). The expression of Klotho was suppressed by miR-199a through direct binding to the three prime untranslated regions (3'-UTR). The high miR-199a level was accompanied by low Klotho expression in the LN kidney. MiR-199a promoted LPS-induced NF-κB activation and improved the secretion of TNF-α and IL-1β by regulation of Klotho in HEK293âT cells. If miR-199a antagomir was administrated after 48âh of pristane administration, the expression of p-P65 and the secretion of TNF-α and IL-1β were significantly down-regulated in LN kidney. Although the direct involvement and detailed mechanism of miR-199a in LN still need further investigation, our data show that MiR-199a could regulate the activation of NF-κB by directly targeting Klotho.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 103, November 2018, Pages 235-242
Journal: Molecular Immunology - Volume 103, November 2018, Pages 235-242
نویسندگان
Hong Ye, Bofeng Su, Haizhen Ni, Linlin Li, Xuduan Chen, Xiaohan You, Huidi Zhang,