MicroRNAs induced by IFNα in HepG2 cells
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ABSTRACT:
PROVIDER: PRJNA1311834 | ENA |
REPOSITORIES: ENA
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Project description:Interferon-α (IFNα) plays a key role in innate immunity by inducing interferon-stimulated genes (ISGs). Beyond protein-coding ISGs, non-coding RNAs such as microRNAs are also modulated by IFNα. Here, we profiled differentially expressed microRNAs in HepG2 cells following IFNα stimulation, providing new insights into interferon signaling and antiviral regulation.
2025-09-09 | GSE306696 | GEO
Project description:Purpose: Using RNA-seq to analyze the different expressions induced by IFNα among the SETD2-KO HepG2 cells, STAT1-KO HepG2 cells and STAT1-K525A-Re HepG2 cells and HepG2 control cells Methods: mRNA profiles of HepG2 control cells and SETD2-KO cells, STAT1-KO cells, STAT1-K525A-Re cells were generated by deep sequencing, using BGISEQ-500RS. The sequence reads that passed quality filters were analyzed at the transcriptional level with RSEM (RNA-seq by Expectation Maximization).
2019-03-12 | GSE98372 | GEO
Project description:In order to identify IFNα-induced host factor(s) that might inhibit replication of unadapted chimeric SIV/HIV-1 viruses (SHIVs), we measured IFNα-induced gene expression in immortalized pig-tailed macaque (Ptm) CD4+ lymphocytes. Triplicate cultures of Ptm lymphocytes were left untreated or treated with 1000 U/ml of IFNα. Twenty-four hours later, RNA was isolated, and RNA-seq libraries were prepared for sequencing. A total of 198 genes were found to be significantly differentially expressed (|logFC| ≥ 0.585 & FDR 5%) upon IFNα treatment. 147/198 genes were found to be significantly upregulated and 51/198 genes were found to be significantly downregulated regulated upon IFNα treatment.
2019-06-24 | GSE126594 | GEO
Project description:Different expressed microRNAs in exosome from HepG2 cells regulated by PBLD
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Project description:Cancer treatments have been revolutionized by the emergence of immune checkpoint blockade therapies. However, only a minority of patients with various tumor types have benefited from such treatments. New strategies focusing on the immune contexture of the tumor tissue microenvironment hold great promises. Here, we created IFNα-overexpressing mesenchymal stromal cells (IFNα-MSCs). Upon direct injection into tumors, we found that these cells are powerful in eliminating several types of tumors. Interestingly, the intra-tumoral injection of IFNα-MSCs could also induce specific anti-tumor effects on distant tumors. These IFNα-MSCs promoted tumor cells to produce CXCL10, which in turn potentiates the infiltration of CD8+ T cells in the tumor site. Furthermore, IFNα-MSCs enhanced the expression of granzyme B (GZMB) in CD8+ T cells and invigorated their cytotoxicity in a Stat3-dependent manner. Genetic ablation of Stat3 in CD8+ T cells impaired the effect of IFNα-MSCs on GZMB expression. Importantly, combination of IFNα-MSCs and PD-L1 blockade induced an even stronger anti-tumor immunity. Therefore, IFNα-MSCs represent a novel tumor immunotherapy strategy, especially when combined with PD-L1 blockade.
2021-10-31 | GSE184918 | GEO
Project description:Compare microRNAs expression when HepG2 cells stably expressing HBx protein with HepG2 control cells expressing baterial chloramphenicol acetyltransferase Compare microRNAs expression when HepG2 cells stably expressing URG11 protein with HepG2 control cells expressing baterial chloramphenicol acetyltransferase microRNA expression in Cells expressing HBx vs. Cell without HBx microRNA expression in Cells expressing URG11 vs. Cell without URG11
2011-11-23 | E-GEOD-33854 | biostudies-arrayexpress
Project description:The cause of systemic lupus erythematosus (SLE) is unknown. Interferonα (IFNα) has been suggested as a causative agent of SLE, however, it is not proven, and to what extent and how IFNα contributes to the disease is unknown. We here directly studied the contribution of IFNα to SLE by generating inducible IFNα transgenic mice which showed that conditional up-regulation of IFNα induced a typical manifestation of SLE including serum immune complex (IC), autoantibody against double stranded DNA (anti-dsDNA Ab) and the organ manifestations classical to SLE such as IC-deposited glomerulonephritis, classical splenic onion-skin lesion, and alopecia, epidermal liquefaction, positive lupus-band test of the skin. In the spleen of mice, activated effector CD4 T cells, interferonγ-producing CD8 T cells, B220+CD86+ cells and CD11c+CD86+ cells were increased, and the T cells produced increased amounts of IL-4, IL-6, IL-17 and IFNγ and decreased IL-2. In particular, activated CD3+CD4-CD8- double-negative T (DNT) cells positive for TCRαβ, B220, CD1d-teteramer, PD-1 and Helios, which produced increased amounts of IFNγ, IL-4, IL-17 and TNFα, were significantly expanded. They infiltrated into kidney and induced de novo glomerulonephritis and alopecia when transferred into naïve recipients. Thus, conditional up-regulation of IFNα is sufficient to induce SLE, and the DNT cells as expanded by IFNα are directly responsible for the organ manifestations such as lupus skin disease or nephritis.
2018-12-10 | GSE123549 | GEO
Project description:Apolipoprotein A-I mimetic peptides are amphipathic alpha-helix peptides that display similar functions to apolipoprotein A-I. Preclinical and clinical studies have demonstrated the safety and efficacy of apolipoprotein A-I mimetic peptides in multiple indications associated with inflammatory processes. In this study, we evaluated the effect of the long-term expression of L37pA in the liver by an adeno-associated virus (AAV-L37pA) on the expression of an adeno-associated virus encoding interferon-alpha (AAV-IFNα). Long-term IFNα expression in the liver leads to lethal hematological toxicity one month after AAV administration. Concomitant administration of AAV-L37pA prevented the lethal toxicity since the IFNα expression was reduced one month after AAV administration by decreasing the expression of IFNα. To identify the mechanism of action of L37pA, a genomic and proteomic analysis was performed fifteen days after AAV administration when a similar level of IFNα and interferon-stimulated genes were observed in mice treated with AAV-IFNα alone and in mice treated with AAV-IFNα and AAV-L37pA. The coexpression of the apolipoprotein A-I mimetic peptide L37pA with IFNα modulated the gene expression program of IFNα, inducing a significant reduction in inflammatory pathways affecting pathogen-associated molecular patterns receptor, dendritic cells, NK cells and Th1 immune response. The proteomic analysis confirmed the impact of the L37pA activity on several inflammatory pathways and indicated an activation of LXR/RXR and PPPARα/γ nuclear receptors. Thus, long-term expression of L37pA induces an anti-inflammatory effect in the liver that allows silencing of IFNα expression mediated by an adeno-associated virus.
2021-09-09 | PXD023281 | Pride
Project description:Different expressed microRNAs in exosome from HepG2 cells by comparing the PBLD-overexpression group and the control group.
2022-11-11 | GSE185879 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE17299: Direct effects of IFNα on human CD8 T cells_without any other concomitant signals GSE17301: The effect of IFNα on human CD8 T cells_with other concomitant signals Refer to individual Series
2010-07-23 | E-GEOD-17302 | biostudies-arrayexpress