Analysis of host response to the infected Clonorchis sinensis metacercariae and adult worm. The infected tissues evidenced altered expression of genes involved in systems such as immune response and cell cycle regulation, as compared with normal tissues.
Gene expression profiling in mouse liver infected with Clonorchis sinensis metacercariae.
Sex, Specimen part
View SamplesWe observed that transcriptional activity and the number of active genes were significantly correlated with the distribution of 8-oxoG in gene promoter regions, as determined by liquid chromatography/mass spectrometry (LC/MS), and 8-oxoG and RNA sequencing Overall design: RNA-sequencing of lung and adipose tissues isolated from two juvenile female C57BL/6 mice
8-OxoG in GC-rich Sp1 binding sites enhances gene transcription in adipose tissue of juvenile mice.
Sex, Age, Specimen part, Cell line, Subject
View SamplesMicroglia activation contributes to the development of neuropathic pain.
High-resolution transcriptome analysis reveals neuropathic pain gene-expression signatures in spinal microglia after nerve injury.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Posttranscriptional crossregulation between Drosha and DGCR8.
No sample metadata fields
View SamplesAnaysis of mRNA changes in HeLa cells following knockdown of Drosha or DGCR8. Drosha is a nuclear RNase III that carries out microRNA (miRNA) processing by cleaving primary microRNA transcript (pri-miRNA). DGCR8 is an essential co-factor of Drosha.
Posttranscriptional crossregulation between Drosha and DGCR8.
No sample metadata fields
View SamplesAnalysis of mRNA changes in HeLa cells following Ago2 or Dicer depletion. Dicer, a cytoplasmic RNase III, generates the mature form of small RNAs including microRNA. Ago2 is a component of an effector complex of microRNA.
Posttranscriptional crossregulation between Drosha and DGCR8.
No sample metadata fields
View SamplesTo determine the genes potentially responsible for the lactate-mediated gene expression regulation in hepatocellular carcinoma, we performed RNA-seq analyses on parental HepG2, HepG2/metR and oxamate-treated HepG2/metR cells. To gain mechanistic insights into the lactate-induced pro-migratory phenotypes, we established a cell model that acquired a resistance to metformin while producing lactate at a high level by selecting HepG2 cells that survived a chronic exposure to metformin for more than 5 months (HepG2/metR). In HepG2/metR cells, glycolysis rates were increased by more than 3 folds compared with parental cells, and consequently, lactate production was also highly enhanced. To clarify the gene expression regulation between the lactate level in the HepG2/metR model, we treated the cells with oxamate, an inhibitor of lactate dehydrogenase, and found that it significantly. Using a 2-fold change cut-off value in transcriptome, we selected 1,757 genes significantly up-regulated in HepG2/metR vs parental HepG2 cells. 690 genes were down-regulated by oxamate treatment in HepG2/metR cells. Eventually, we selected 136 genes that are common in the two gene sets, which may directly respond to lactate signaling Overall design: mRNA profiles of HepG2 cells, HepG2/metR (hyper-glycolytic cell model), oxamate treated HepG2/metR (decreased lactate concentration cell) were generated by deep sequencing using Illumina Nextseq 500
Lactate Activates the E2F Pathway to Promote Cell Motility by Up-Regulating Microtubule Modulating Genes.
Specimen part, Cell line, Treatment, Subject
View SamplesPro-inflammatory response of VSMCs is triggered by endothelial damage and a causative step for thrombosis and neointimal thickening in the arterial vessels. Therefore, we investigate a role of cytosolic Hsp60 as a novel pro-inflammatory mediator in VSMCs. Hsp60 was detected in the cytosol of VSMCs. The selective depletion of cytosolic Hsp60 in VSMCs reduced the IKK activation, repressed the induction of NF-?B-dependent pro-survival genes (MnSOD and Bfl-1/A1), and enhanced apoptotic death in response to TNF-a. Moreover, a quantitative RNA sequencing revealed that the expression of 75 genes among the 774 TNF-a-inducible genes was significantly reduced by the depletion of cytosolic Hsp60. In particular, the expression of pro-inflammatory cytokines/chemokines, such as CCL2, CCL20, and IL-6, was regulated by the cytosolic Hsp60 in VSMCs. Finally, the depletion of cytosolic Hsp60 markedly inhibited the neointimal thickening in the balloon-injured arterial vessels by inducing apoptotic cell death and inhibiting chemokine production. This study provides the first evidence that cytosolic Hsp60 could be a therapeutic target for preventing inflammation-driven VSMC hyperplasia in the injured vessels. Overall design: Hsp60 normal vs knockout with TNF-alpha treatment
Cytosolic Hsp60 orchestrates the survival and inflammatory responses of vascular smooth muscle cells in injured aortic vessels.
No sample metadata fields
View SamplesInhalation of toxic chemicals, including recent e-cigarettes, often cause life-threatening lung injury. Although exposure to polyhexamethylene guanidine (PHMG)-containing humidifier disinfectant (HD) has been identified as a cause of fatal lung injury, the mechanism underlying HD-associated lung injury (HDLI) is unknown. The present study evaluated global changes in gene expression in lung tissues from patients with PHMG-induced HDLI, and compared gene expression changes in PHMG-induced rat lung tissues. Significantly different expressions in lung tissues between patients with HDLI and unaffected controls were observed. Furthermore, several fibrosis-associated overlapping genes (such as MMP2 and COL1A2) shared between humans with HDLI and rats exposed to PHMG were identified. Interactome network analysis predicted different pathways between children and adults with HDLI: the TGFβ/SMAD signaling pathway was central in adults, whereas other pathways, including integrin signaling, were associated with HDLI in children. Further interactome network analysis revealed that Rap1 and CCKR signaling pathways were significantly enriched in HDLI compared with idiopathic pulmonary fibrosis as well as their recapitulation in the lung tissues of rats exposed to PHMG. Our results suggest that MMP2-mediated different mechanisms between children and adults may be associated with PHMG-induced HDLI development, and Rap1 and CCKR pathways appear to be crucial.
Integrative multi-omics approach for mechanism of humidifier disinfectant-associated lung injury.
Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A lactate-induced response to hypoxia.
Specimen part, Cell line, Treatment
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