MiR-146b-5p targets IFI35 to inhibit inflammatory response and apoptosis via JAK1/STAT1 signalling in lipopolysaccharide-induced glomerular cells
| Autor: | Jian-Ying Chen, Sheng-Zhi Jiang, Xia Guo, Qiao Li, Jie-Rou Huang, Hui Rao, Li-Hua Zhang, Bin Xiao |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Lipopolysaccharides
Lipopolysaccharide biology medicine.diagnostic_test Immunology Cell Apoptosis Molecular biology Proinflammatory cytokine Flow cytometry chemistry.chemical_compound MicroRNAs medicine.anatomical_structure chemistry Western blot microRNA biology.protein medicine Immunology and Allergy Humans STAT1 Interferons Signal Transduction |
| Zdroj: | Autoimmunity. 54(7) |
| ISSN: | 1607-842X |
| Popis: | The dysregulated microRNAs (miRNAs) are implicated in the malignancy of lupus nephritis (LN). This work aims to analyse the effect and mechanism of miR-146b-5p in lipopolysaccharides (LPS)-induced model of LN in vitro. The serum samples of LN patients and normal volunteers were collected. HK-2 cells were challenged via LPS. miR-146b-5p and interferon-induced protein 35 (IFI35) abundances were detected via quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. The inflammatory response was assessed via inflammatory cytokines levels via qRT-PCR and enzyme-linked immunosorbent assay. Cell apoptosis was analysed via flow cytometry and apoptotic protein levels. The protein levels of JAK1/STAT1 signalling were detected via western blot. The relationship of miR-146b-5p and IFI35 was analysed via bioinformatics and dual-luciferase reporter assays. This study revealed that miR-146b-5p level was declined and IFI35 abundance was elevated in serum of LN patients and LPS-challenged HK-2 cells. Functionally, IFI35 overexpression promoted LPS-caused inflammatory response and cell apoptosis, and knockdown of IFI35 caused an opposite trend. Meanwhile, miR-146b-5p targeted IFI35 to suppress inflammatory response and cell inflammatory response and apoptosis via inactivating the JAK1/STAT1 pathway. MiR-146b-5p suppressed inflammatory response and cell apoptosis by IFI35 mediated-JAK1/STAT1 signalling in HK-2 cells, which provided a new mechanism for understanding the pathogenesis of LN. |
| Databáze: | OpenAIRE |
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