We focused on how mica fine particle influences macrophage activities.
Modulation of macrophage activities in proliferation, lysosome, and phagosome by the nonspecific immunostimulator, mica.
Specimen part, Cell line
View SamplesTo investigate the role of ADAR1 in gastric carcinogenesis, RNA sequencing and small RNA sequencing were performed in AGS and MKN-45 cells with stable ADAR1 knock-down. Changed frequencies of editing and messenger RNA (mRNA) and microRNA (miRNA) expression were then identified by bioinformatic analyses. Overall design: mRNA and miRNA sequencing were performed before and after stable knockdown of ADAR1 in AGS and MKN-45 cell line
Combinatory RNA-Sequencing Analyses Reveal a Dual Mode of Gene Regulation by ADAR1 in Gastric Cancer.
No sample metadata fields
View SamplesMacrophages have distinct characteristics depending on their microenvironment. We performed proteomic analysis between M1 and M2 macrophages and found that cellular metabolism is the key regulator of macrophage function.
Proteomic Analysis Reveals Distinct Metabolic Differences Between Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) and Macrophage Colony Stimulating Factor (M-CSF) Grown Macrophages Derived from Murine Bone Marrow Cells.
Specimen part
View SamplesBlood-retina barrier (BRB) formation and retinal angiogenesis depend on beta-catenin signaling induced by the ligand norrin (NDP), the receptor frizzled4 (FZD4), co-receptor LRP5, and the tetraspanin TSPAN12. Impaired NDP/FZD4 signaling causes familial exudative vitreoretinopathy (FEVR), which may lead to blindness. Endothelial-cell specific inactivation of the Tspan12 gene at P28 using a Cdh5-CreERT2 driver shows that TSPAN12 functions in ECs to promote vascular morphogenesis and BRB formation in developing mice, and BRB maintenance in adult mice. 12 month after Tspan12 inactivation and loss of BRB maintenance with massive IgG and albumin extravasation we observe complement activation, cystoid edema, and impaired beta-wave in electroretinograms. RNA-Seq 6 month after Tspan12 inactivation provides a detailed view on the transcriptional response, including activation of antibody effector systems (complement and Fc receptors), inflammation and microglia responses, extracellular matrix organization and remodeling, and other responses. Overall design: Endothelial cell-specific inactivation of floxed Tspan12 was induced at P28 using a Cdh5-CreERT2 driver and total retina RNA (ribodepleted) from 4 control or ECKO retinas (8 samples) was subjected to RNA-Seq 6 months later
Endothelial Cell-Specific Inactivation of TSPAN12 (Tetraspanin 12) Reveals Pathological Consequences of Barrier Defects in an Otherwise Intact Vasculature.
Specimen part, Cell line, Subject
View SamplesSevere fever with thrombocytopenia syndrome phlebovirus (SFTSV), listed in the WHO most dangerous pathogens, has 12-30% fatality rates with a characteristic thrombocytopenia syndrome. With a majority of clinically diagnosed SFTSV patients older than ~50 years, age is a critical risk factor for SFTSV morbidity and mortality. Here, we report an age-dependent ferret model of SFTSV infection and pathogenesis that fully recapitulates the clinical manifestations of human infections. While young adult ferrets (=2 years old) did not show any clinical symptoms and mortality, SFTSV-infected aged ferrets (=4 years old) demonstrated severe thrombocytopenia, reduced white blood cells, and high fever with 93% mortality rate. Moreover, significantly higher viral load was observed in aged ferrets. Transcriptome analysis of SFTSV-infected young ferrets revealed strong interferon-mediated anti-viral signaling, whereas inflammatory immune responses were markedly upregulated and persisted in aged ferrets. Thus, this immunocompetent age-dependent ferret model should be useful for anti-SFTSV therapy and vaccine development. Overall design: Two groups of young adults (20-24 months, =2Y) and aged ferrets (48-50 months), =4 Y) were inoculated via the IM route with 107.6 TCID50 of the SFTSV CB1/2014 strain. PBMCs were isolated at 2 and 4 dpi from each group of ferrets (n=3) by density gradient centrifugation using Ficoll-Paque Plus according to the manufacture's protocol.
Ferret animal model of severe fever with thrombocytopenia syndrome phlebovirus for human lethal infection and pathogenesis.
Specimen part, Subject
View SamplesWe performed high throughput RNA sequencing at preadipocyte (D0) and differentiated adipocyte (D7) of primary brown preadipocyte and found that Kruppel-like factor 16 (KLF11) gene that was downregulated in D7 was a novel negative regulator of adipogenesis. Overall design: To explore global view of gene expression during adipogenesis, RNA-seq was performed in the primary cultured brown preadipocyte (D0) and brown adipocyte after 7 day differentiation (D7). Compared with D0, 6,668 genes were identified as 2 fold differentially expressed genes (DEGs) at D7 including 2,836-upregulated genes and 3,832 down-regulated genes.
RNA-Seq Analysis Reveals a Negative Role of KLF16 in Adipogenesis.
Specimen part, Cell line, Subject
View SamplesGPCR19 pathway has been implicated in regulating various inflammation. However, the exact mechanism of immune regulation by GPCR19 pathway has not been elucidated in detail.
Taurodeoxycholate Increases the Number of Myeloid-Derived Suppressor Cells That Ameliorate Sepsis in Mice.
Sex, Specimen part
View SamplesPrenatal alcohol exposure can cause long-lasting changes in functional and genetic programs of the brain, which may underlie behavioral alterations found in FASD.
Ethanol-related alterations in gene expression patterns in the developing murine hippocampus.
Specimen part
View SamplesCancer cell phenotypes are partially determined by epigenetic specifications such as DNA methylation. Metastasis development is a late event in cancerogenesis and might be associated with epigenetic alterations. Here, we analyzed genome wide DNA methylation changes that were associated with pro-metastatic phenotypes in non-small cell lung cancer with Reduced Representation Bisulfite Sequencing. DNMT-inhibition by 5-Azacytidine at low concentrations reverted the pro-metastatic phenotype. 5-Azacytidine led to preferential loss of DNA methylation at sites that were DNA hypermethylated during the in vivo selection. Changes in DNA methylation persisted over time.
DNA methyltransferase inhibition reverses epigenetically embedded phenotypes in lung cancer preferentially affecting polycomb target genes.
Cell line
View SamplesExhausted T cells express multiple co-inhibitory molecules that impair their function and limit immunity to chronic viral infection. Defining novel markers of exhaustion is important both for identifying and potentially reversing T cell exhaustion. Herein, we show that the ectonucleotidse CD39 is a marker of exhausted CD8+ T cells. CD8+ T cells specific for HCV or HIV express high levels of CD39, but those specific for EBV and CMV do not. CD39 expressed by CD8+ T cells in chronic infection is enzymatically active, co-expressed with PD-1, marks cells with a transcriptional signature of T cell exhaustion and correlates with viral load in HIV and HCV. In the mouse model of chronic Lymphocytic Choriomeningitis Virus infection, virus-specific CD8+ T cells contain a population of CD39high CD8+ T cells that is absent in functional memory cells elicited by acute infection. This CD39high CD8+ T cell population is enriched for cells with the phenotypic and functional profile of terminal exhaustion. These findings provide a new marker of T cell exhaustion, and implicate the purinergic pathway in the regulation of T cell exhaustion.
CD39 Expression Identifies Terminally Exhausted CD8+ T Cells.
Specimen part, Subject
View Samples