Ambion and Exiqon miRNA profiling
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens
PROVIDER: GSE16638 | GEO | 2015/01/01
SECONDARY ACCESSION(S): PRJNA116217
REPOSITORIES: GEO
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Project description:The goal of this experiment was to determine gene expression changes during influenza A virus infection as the result of expression influenza virus inducible miRNAs in A549 cells. The gene expression profiling experiment was performed with 4 groups (mock infected, influenza A virus infected, influenza A virus infected in the presence of exogenous miR-141, miR-374b, miR-449b, miR-518b, and miR-1263, and influenza A virus infected in the presence of exogenous miR-147b, miR-190b, miR-199a, miR-512-5p, and miR-874 with 3 biological replicates for each group. Total RNA was purified from A549 cells that were mock infected or infected with influenza A virus (A/WSN/33, 5pfu/cell) alone or in the presence of miRNA mimics 10 hours after treatment.
2013-09-15 | E-GEOD-47937 | biostudies-arrayexpress
Project description:Antiviral responses must be regulated to rapidly defend against infection while minimizing inflammatory damage, but the mechanisms for establishing the magnitude of response within an infected cell are not well understood. miRNAs are small non-coding RNAs that negatively regulate protein levels by binding target sequences on their cognate mRNA. Here we identify miR-144 as a negative regulator of the host antiviral response. Ectopic expression of miR-144 resulted in increased replication of three RNA viruses, influenza, EMCV, and VSV, in primary mouse lung epithelial cells. To elucidate the mechanism whereby miR-144 increases influenza replication within lung epithelial cells, immortalized murine Type I epithelial cells (Let1 cells) stably over-expressing miR-144 were infected with influenza A for 1 or 18 hours and the transcriptional profile was compared with those of infected control cells. This systems biology approach identified the transcriptional network regulated by miR-144 and demonstrated that it controls the TRAF6/IRF7 antiviral response by post-transcriptionally suppressing TRAF6 levels. In vivo ablation of miR-144 reduced influenza replication within the lung. 16 RNA samples from immortalized murine Type I airway epithelial cells (Let1 cells) were analyzed using Agilent microarrays. Cells expressing miR-144, miR-451, or a vector control (GFP) were analyzed after infection with PR8 influenza virus (MOI=5) for 1 or 18 hours.
2013-09-11 | E-GEOD-50742 | biostudies-arrayexpress
Project description:Virus infection may shut off host protein synthesis in order to achieve the replicative advantage over host cells. It is well known that human pathogenic viruses, particularly the picornaviruses, can block host protein synthesis by cleavage or inhibition of eukaryotic initiation factors (eIFs). In this study we found a novel mechanism that microRNA (miRNA) is involved in viral pathogenesis. Infection of enteroviruses can disturb the expression of host miRNAs, in which miR-141 is up-regulated and inhibits host protein synthesis by post-transcriptional repression of the target gene eIF4E, a key element for cap-dependent translation of host proteins. Knockdown of miR-141 by a specific siRNA, antagomiR-141, could restore host eIF4E expression, delay the occurrence of cytopathic effect (CPE), and impair virus propagation. We demonstrated that EV71 infection could increase early growth response 1 (EGR1) expression which induced miR-141 causing the eIF4E suppression; while silencing of EGR1 attenuated virus production. Our results suggest that enterovirus infection causes the EGR1-mediated upregulation of host miR-141, further lead to the translational switch from cap-dependent to cap-independent protein synthesis in the host cells, an environmental beneficial for viral propagation. This novel mechanism may highlight a new approach for future development of antiviral therapy.
2011-01-03 | GSE15323 | GEO
Project description:Fibroblast growth factor (FGF) 2 (FGF2 or basic FGF) mediates a wide range of biological functions, such as regulating proliferation, angiogenesis, migration, differentiation and injury repair. However, the roles of FGF2 and the underlying mechanisms of action in influenza virus (IAV) -induced lung injury remain largely unexplored. In this study, we firstly report miR-194 expression is significantly decreased in A549 cells following influenza virus A/Beijing/501/2009 (BJ501) infection. MiR-194 directly targeting FGF2, a novel antiviral regulator, could suppress FGF2 expression both in mRNA and protein levels. Overexpression miR-194 facilitate IAV replication via negatively regulating type I IFN production, and reintroduction of FGF2 abrogates miR-194-induced effects on promoting IAV replication. On the contrary, inhibition of miR-194 alleviate IAV induced lung injury via promoting type I IFNs antiviral activities in vivo. Importantly, contrary to FGF2 activated RIG-I signaling pathway, miR-194 suppressed TBK1 and IRF3 phosphorylation. Taken together, our findings demonstrated that miR-194-FGF2 axis play a vital role in IAV-induced lung injury, and miR-194 antagonism might be as a potential therapeutic target during IAV infection. Fibroblast growth factor (FGF) 2 (FGF2 or basic FGF) mediates a wide range of biological functions, such as regulating proliferation, angiogenesis, migration, differentiation and injury repair. However, the roles of FGF2 and the underlying mechanisms of action in influenza virus (IAV) -induced lung injury remain largely unexplored. In this study, we firstly report miR-194 expression is significantly decreased in A549 cells following influenza virus A/Beijing/501/2009 (BJ501) infection. MiR-194 directly targeting FGF2, a novel antiviral regulator, could suppress FGF2 expression both in mRNA and protein levels. Overexpression miR-194 facilitate IAV replication via negatively regulating type I IFN production, and reintroduction of FGF2 abrogates miR-194-induced effects on promoting IAV replication. On the contrary, inhibition of miR-194 alleviate IAV induced lung injury via promoting type I IFNs antiviral activities in vivo. Importantly, contrary to FGF2 activated RIG-I signaling pathway, miR-194 suppressed TBK1 and IRF3 phosphorylation. Taken together, our findings demonstrated that miR-194-FGF2 axis play a vital role in IAV-induced lung injury, and miR-194 antagonism might be as a potential therapeutic target during IAV infection.
2017-08-24 | GSE103009 | GEO
Project description:Virus infection may shut off host protein synthesis in order to achieve the replicative advantage over host cells. It is well known that human pathogenic viruses, particularly the picornaviruses, can block host protein synthesis by cleavage or inhibition of eukaryotic initiation factors (eIFs). In this study we found a novel mechanism that microRNA (miRNA) is involved in viral pathogenesis. Infection of enteroviruses can disturb the expression of host miRNAs, in which miR-141 is up-regulated and inhibits host protein synthesis by post-transcriptional repression of the target gene eIF4E, a key element for cap-dependent translation of host proteins. Knockdown of miR-141 by a specific siRNA, antagomiR-141, could restore host eIF4E expression, delay the occurrence of cytopathic effect (CPE), and impair virus propagation. We demonstrated that EV71 infection could increase early growth response 1 (EGR1) expression which induced miR-141 causing the eIF4E suppression; while silencing of EGR1 attenuated virus production. Our results suggest that enterovirus infection causes the EGR1-mediated upregulation of host miR-141, further lead to the translational switch from cap-dependent to cap-independent protein synthesis in the host cells, an environmental beneficial for viral propagation. This novel mechanism may highlight a new approach for future development of antiviral therapy. Enteroviruses in the Picornaviridae family are important human pathogens which can cause fatal diseases, including cardiopulmonary failure, aseptic meningitis, paralysis, myocarditis, and encephalomyelitis. Virus infection may induce shutoff of host protein synthesis, particularly in picornavirus, whose protein translation is cap-independent. It is known that poliovirus 2A protease cleaves eIF4G, a scaffold component of mammalian cell translational complex, leading to the shut down of host protein synthesis. Nevertheless, the cleavage of eIF4G may not be sufficient for the complete shutoff of host protein synthesis. Previous studies showed that cleavage of polyA-binding protein (PABP) by viral protease 3C and dephosphorylation of the translational repressor, eIF4E binding protein 1 (4E-BP1), also contribute to this process. The cap-binding protein, eIF4E, is the most crucial factor in determining whether cap-dependent or -independent translation takes place. The mechanism by which viral infection modulates host cell protein synthesis through interfering eIF4E expression is not yet known. miRNAs are a newly discovered class of small non-protein-coding RNAs that may act via endogenous RNA interference. Our understanding of its role in the dynamic interplay between virus and host components is quite limited. Since both virus infection and miRNAs could hinder cellular protein synthesis, whether miRNAs are involved during virus infection in shutting off host protein synthesis is still unknown. To address this issue, we analyze the altered gene and microRNA expression after EV71 infection. ***This submission represents the mRNA expression component of the study only***
2011-01-03 | E-GEOD-15323 | biostudies-arrayexpress
Project description:Virus-host interactions are complicated processes, and multiple cellular proteins have been reported to promote or inhibit viral replication through different mechanisms. Recent progress has implicated circular RNAs (circRNA) in cancer biology and progression; however, the role of circRNAs in viral infection remains largely unclear. Here, we detected 11,620 circRNAs in A549 cells and found that 411 of them were differentially expressed in influenza virus-infected A549 cells. We characterized a novel intronic circRNA, AIVR, that was upregulated in influenza virus-infected A549 cells, and found that silencing of AIVR significantly promoted influenza virus replication in A549 cells. We further found that AIVR predominantly localizes in the cytoplasm and works as a microRNA (miRNA) sponge. One of the miRNAs absorbed by AIVR binds the mRNA of CREBBP, which is an important component of the large nucleoprotein complex IFN-β enhanceosome that accelerates IFN-β production. AIVR-overexpression significantly increased the mRNA and protein levels of INF-β in the influenza virus-infected A549 cells. Therefore, the upregulation of AIVR is a cellular antiviral strategy, with AIVR exerting its antiviral effect by absorbing miRNA and promoting the expression of CREBBP to facilitate IFN-β production. Our study provides new insights into the roles of circRNAs in the cellular innate antiviral response.
2021-07-06 | GSE172315 | GEO
Project description:Small RNAs were profiled during influenza A virus infection of human A549 cells to identify changes in microRNA abundance during the cellular antiviral response. Examination of microRNA abundance during influenza A virus infection.
2013-09-15 | E-GEOD-48036 | biostudies-arrayexpress
Project description:We performed RNA sequencing of islets of Langerhans isolated from RipmiR-141~200c and RipmiR-141~200c Zeb1200M mice to determine the transcriptomic effects of mutating miR-200 binding sites in the endogenous Zeb1 3'UTR of mice in which miR-141~200c is overexpressed under the rat insulin promoter (RIP).
2022-04-30 | E-MTAB-10537 | biostudies-arrayexpress
Project description:CD47 is an ubiquitously expressed surface molecule that has a significant impact on immune responses. However, its role for antiviral immunity is not fully understood. We can show that CD47 has an inhibitory role in influenza virus defense, since CD47-deficient mice (CD47-/-) display an increased viral clearance during influenza virus infection. This effect is strongly associated with alveolar macrophages, yet the underlying mechanisms are unclear. Thus, to assess the precise impact of CD47 on antiviral action of alveolar macrophages, transcriptional analysis of ex vivo isolated alveolar macrophages from CD47-/- and WT mice were performed isolated 3dpi. Surprisingly, instead of classical antiviral mediators, an increased expression of both hemoglobin α and hemoglobin β was found in CD47 deficient compared to WT alveolar macrophages upon influenza A virus infection. Importantly, antiviral activity of hemoglobin was already shown for other viruses and thus, CD47 might limit influenza virus defense via the regulation of hemoglobin, which could act as a modulator of the antiviral immune response during the infection.
2022-12-09 | GSE201825 | GEO
Project description:Antiviral responses must be regulated to rapidly defend against infection while minimizing inflammatory damage, but the mechanisms for establishing the magnitude of response within an infected cell are not well understood. miRNAs are small non-coding RNAs that negatively regulate protein levels by binding target sequences on their cognate mRNA. Here we identify miR-144 as a negative regulator of the host antiviral response. Ectopic expression of miR-144 resulted in increased replication of three RNA viruses, influenza, EMCV, and VSV, in primary mouse lung epithelial cells. To elucidate the mechanism whereby miR-144 increases influenza replication within lung epithelial cells, TC-1 cells stably over-expressing miR-144 were infected with influenza A for 24 hours and the transcriptional profile was compared with those of infected control cells. This systems biology approach identified the transcriptional network regulated by miR-144 and demonstrate that it controls the TRAF6/IRF7 antiviral response by post-transcriptionally suppressing TRAF6 levels. In vivo ablation of miR-144 reduced influenza replication within the lung. TC-1 lung epithelial cells stably expressing miR144+miR451 or control vector were unstimulated (n=1) or infected with Influenza A/PR/8/34 (MOI=5) for 24 hours (n=3).
2012-07-31 | E-GEOD-31955 | biostudies-arrayexpress