Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA306750 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The molecular pathogenesis of infection by HIV (human immunodeficiency virus) is extremely complex and is not clearly defined despite intensive research efforts. MiRNA as a class of regulators in cancer development can affect multiple gene pathways by targeting various mRNAs. Thus, studies aimed at transcription and regulation after antiviral treatment combined with beneficial researches related to miRNAs are required. With the purpose of identifying the cascaded miRNA-mRNA regulatory relationships related to infection of HIV in gene level, the parallel miRNA and mRNA expression profiles were analyzed in our study. The differential expressed miRNAs and mRNAs were selected primarily. The differentially regulated miRNA-mRNA interactions were further identified according to the Pearson correlation analysis of gene expression level. In our study, the calculation of the regulatory impact factors (RIF) was also conducted, and it revealed several essential regulators related to antiviral treatment with AIDS. To give a further insight into these TF (transcription factors) regulators, the co-expression gene modules were identified using a threshold-based hierarchical clustering method. Meanwhile, the regulatory network was generated during the computing process. Understanding these regulatory elements may bear significant implications on understanding the pathogenesis of AIDS occurrence.
2023-08-31 | GSE76246 | GEO
Project description:Identification of changes in microRNA expression, remodelling of relationships between microRNA and mRNA expression levels, and genetic polymorphisms associated with inter-individual variation in the dendritic cell immune response to Mycobacterium tuberculosis infection.
2014-01-17 | GSE49951 | GEO
Project description:Identification of changes in microRNA expression, remodelling of relationships between microRNA and mRNA expression levels, and genetic polymorphisms associated with inter-individual variation in the dendritic cell immune response to Mycobacterium tuberculosis infection. We characterised genome-wide changes in microRNA expression, and of the broader miRNA-mdeiated regulatory system, in response to Mycobacterium tuberculosis (MTB) infection, and assessed the extent to which this response is under genetic control. To do so, we profiled microRNA expression levels in primary dendritic cells from 65 individuals before and after infection with MTB for 18 hours.
2014-01-17 | E-GEOD-49951 | biostudies-arrayexpress
Project description:With the purpose of identifying the cascaded miRNA-mRNA regulatory relationships related to infection of HIV in gene level, we extracted mRNA from Peripheral blood mononuclear cells from 50 AIDS patients and 7 uninfected health controls. All AIDS patients in sample were received Antiretroviral Therapy. To further analysis the gene expression pattern in different virus load, we classified high virus loads (HVL, n=14) and low virus loads (LVL, n=16). 2635 and 2826 differentially expressed genes (DEGs) were selected, respectively in LVL and HVL. Functional enrichment analysis indicated DEGs which involved in immune response and apoptosis, played a crucial role in HIV infection. Further, we identified 5 most influential TFs to build miRNA-TF-mRNA regulatory network.
2021-11-10 | GSE140713 | GEO
Project description:With the purpose of identifying the cascaded miRNA-mRNA regulatory relationships related to infection of HIV in gene level, we extracted mRNA from Peripheral blood mononuclear cells from 50 AIDS patients and 7 uninfected health controls. All AIDS patients in sample were received Antiretroviral Therapy. To further analysis the miRNA expression pattern in different virus load, we classified high virus loads (HVL, n=14) and low virus loads (LVL, n=16). 145 and 129 differentially expressed miRNAs (DEMs) were selected, respectively in LVL and HVL. Functional enrichment analysis indicated miRNA-correlated targets which involved in immune response and apoptosis, played a crucial role in HIV infection. Further, we identified 5 most influential TFs to build miRNA-TF-mRNA regulatory network.
2021-11-10 | GSE140650 | GEO
Project description:Matrix metalloproteinase-9 (MMP-9) expression is up-regulated in alveolar macrophages (AM) of HIV1+ smokers who develop emphysema. Based on the knowledge that lung epithelial lining fluid (ELF) of HIV1+ smokers has increased levels of inflammatory cytokines compared to HIV1- smokers, we hypothesized up-regulation of lung cytokines in HIV1+ smokers may be functionally related to increased MMP-9 expression. Cytokine arrays evaluated cytokine protein levels in ELF obtained from 5 groups of individuals: HIV1‾ healthy nonsmokers, HIV1‾ healthy smokers, HIV1‾ smokers with low diffusing capacity (DLCO) , HIV1 + nonsmokers, and HIV1 + smokers with low DLCO. Among several pro-inflammatory cytokines elevated in ELF associated with smoking and HIV1+, increased levels of the Th17-related cytokine IL-23 were found in HIV1- smokers with low DLCO and HIV1+ smokers and nonsmokers. Relative IL-23 gene expression was significantly increased in AM of HIV1+ individuals, with greater expression in AM of HIV1+ smokers with low DLCO. Infection with HIV1 in vitro induced IL-23 expression in normal AM. Since AM purified by adherence contain a small number of lymphocytes, we hy-pothesized that in an AM/lymphocyte co-culture system, IL-23 would up-regulate MMP-9. IL-23 stimulation of AM/lymphocyte co-cultures in vitro induced increased MMP-9 mRNA levels and protein. AM of healthy individuals did not express IL-23 receptors (IL-23R), lung T lymphocytes express IL-23R and interact with AM in order to up-regulate MMP-9. This mechanism may contribute to the increased tissue destruction in the lungs of HIV1+ smokers and suggests that Th-17 related inflammation may play a role. IL-23 upregulates MMP-9 expression in human alveolar macrophages via a T lymphocyte/alveolar macrophage interaction, suggesting a possible role for Th-17 related inflammation in accelerated emphysema in HIV1+ smokers.
2024-06-05 | GSE64598 | GEO
Project description:Matrix metalloproteinase-9 (MMP-9) expression is up-regulated in alveolar macrophages (AM) of HIV1+ smokers who develop emphysema. Based on the knowledge that lung epithelial lining fluid (ELF) of HIV1+ smokers has increased levels of inflammatory cytokines compared to HIV1- smokers, we hypothesized up-regulation of lung cytokines in HIV1+ smokers may be functionally related to increased MMP-9 expression. Cytokine arrays evaluated cytokine protein levels in ELF obtained from 5 groups of individuals: HIV1‾ healthy nonsmokers, HIV1‾ healthy smokers, HIV1‾ smokers with low diffusing capacity (DLCO) , HIV1 + nonsmokers, and HIV1 + smokers with low DLCO. Among several pro-inflammatory cytokines elevated in ELF associated with smoking and HIV1+, increased levels of the Th17-related cytokine IL-23 were found in HIV1- smokers with low DLCO and HIV1+ smokers and nonsmokers. Relative IL-23 gene expression was significantly increased in AM of HIV1+ individuals, with greater expression in AM of HIV1+ smokers with low DLCO. Infection with HIV1 in vitro induced IL-23 expression in normal AM. Since AM purified by adherence contain a small number of lymphocytes, we hy-pothesized that in an AM/lymphocyte co-culture system, IL-23 would up-regulate MMP-9. IL-23 stimulation of AM/lymphocyte co-cultures in vitro induced increased MMP-9 mRNA levels and protein. AM of healthy individuals did not express IL-23 receptors (IL-23R), lung T lymphocytes express IL-23R and interact with AM in order to up-regulate MMP-9. This mechanism may contribute to the increased tissue destruction in the lungs of HIV1+ smokers and suggests that Th-17 related inflammation may play a role. IL-23 upregulates MMP-9 expression in human alveolar macrophages via a T lymphocyte/alveolar macrophage interaction, suggesting a possible role for Th-17 related inflammation in accelerated emphysema in HIV1+ smokers.
2024-06-05 | GSE64593 | GEO
Project description:Parallel analysis of mRNA and miRNA expression profiling with AIDS patients
| PRJNA306405 | ENA
Project description:Hantaan virus (HTNV), the prevalent prototype of the hantavirus in Asia, causes hemorrhagic fever with renal syndrome (HFRS) with high mortality in human being. However, the pathogenesis of HTNV infection remains elusive. Accumulating evidences indicate that non-coding RNAs (ncRNAs), including long non-coding RNA (lncRNA), circular RNA (circRNA) and microRNA (miRNA) play crucial roles in the progression of virus infection. Here, we identified differential lncRNA/miRNA/circRNA and mRNA expression profiles of HTNV-infected human umbilical vein endothelial cells (HUVECs) compared with mock-infected HUVECs by whole transcriptome sequencing. Subsequently, comprehensive bioinformatics analyses established miRNA-mRNA co-expression, protein-protein interaction and competing endogenous RNA (ceRNA) networks in miRNA-lncRNA-circRNA-mRNA regulatory axis. The trans or cis regulatory roles of identified RNAs on HTNV infection were ascertained by RNA interference and key ceRNA relationships were verified by dual-luciferase reporter experiments. Moreover, gene ontology (GO) enrichment analysis showed that dysregulated RNAs were mostly related to antiviral innate immune response. In conclusion, our findings firstly revealed that circRNAs and ceRNA network were involved in regulating HTNV infection, and also confirmed several key lncRNAs and miRNAs which had vital effects on HTNV infection. The identification and characterization of RNAs provide the new insights on ceRNA networks in HTNV-host interactions, which lays the foundation for future research of the potential roles of ncRNAs in the pathogenesis of HFRS.
2020-04-06 | GSE133751 | GEO
Project description:Hantaan virus (HTNV), the prevalent prototype of the hantavirus in Asia, causes hemorrhagic fever with renal syndrome (HFRS) with high mortality in human being. However, the pathogenesis of HTNV infection remains elusive. Accumulating evidences indicate that non-coding RNAs (ncRNAs), including long non-coding RNA (lncRNA), circular RNA (circRNA) and microRNA (miRNA) play crucial roles in the progression of virus infection. Here, we identified differential lncRNA/miRNA/circRNA and mRNA expression profiles of HTNV-infected human umbilical vein endothelial cells (HUVECs) compared with mock-infected HUVECs by whole transcriptome sequencing. Subsequently, comprehensive bioinformatics analyses established miRNA-mRNA co-expression, protein-protein interaction and competing endogenous RNA (ceRNA) networks in miRNA-lncRNA-circRNA-mRNA regulatory axis. The trans or cis regulatory roles of identified RNAs on HTNV infection were ascertained by RNA interference and key ceRNA relationships were verified by dual-luciferase reporter experiments. Moreover, gene ontology (GO) enrichment analysis showed that dysregulated RNAs were mostly related to antiviral innate immune response. In conclusion, our findings firstly revealed that circRNAs and ceRNA network were involved in regulating HTNV infection, and also confirmed several key lncRNAs and miRNAs which had vital effects on HTNV infection. The identification and characterization of RNAs provide the new insights on ceRNA networks in HTNV-host interactions, which lays the foundation for future research of the potential roles of ncRNAs in the pathogenesis of HFRS.
2020-04-06 | GSE133634 | GEO