Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA151017 | ENA |
REPOSITORIES: ENA
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Project description:In addition to the role of antioxidant, ascorbic acid (reducing Vitamin C) is an important cofactor for Fe2+ and α-ketoglutarate (α-KG) dependent dioxygenases (Fe2+/α-KGDDs) that comprise many diverse enzymes, including collagen prolyl hydroxylases, jmjC (Jumonji C) domain containing histone demethylases, Ten-eleven translocation (TET) 5-methyl cytosine (5mC) dioxygenases, and N6-methyl adenosine (m6A) demethylase FTO and ALKBH5. Ascorbic acid was reported to induce global epigenetic reprogramming. Here we optimized the library construction flow chart of single-stranded DNA profiling method KAS-seq and utilized KAS-seq to profile transient chromatin states changes upon ascorbic acid treatment for 10 min. We identified several critical pathways affected by ascorbic acid treatment, providing some clues for explaining the reported positive impact of anti-cancer, anti-depression, and anti-obesity for taking ascorbic acid.
2023-07-25 | GSE237843 | GEO
Project description:To characterize target specificity of TETi76, we performed global gene expression analyses of K562TET2+/+ and TET2-/- control cells; TETi76 mimicked expression signatures generated by the loss of TET2 in K562. The addition of Ascorbic Acid (AA), known to enhance TET-dioxygenase activity, counteracted the changes induced by TETi76. In order to study the molecular pathway of synthetic lethality by TET-dioxygenase inhibition, natural TET2-/- mutant cell line SIGM5 was treated with TET inhibitor TETi76 and global gene expression analysis was performed by RNAseq. Result demostrate a significant upregulation of TNT-α signaling and the down regulation of Interferon-α signaling. Interestingly, we also observed significant up-modulation of oxidative stress response pathway genes consistent with the inhibition of dioxygenases. In particular, TETi76 treatment induces 8-fold increase of oxidative stress sensor NQO1 a NRF2 target gene that has been shown earlier to induce pro-apoptotic cell death in cancer cells.
2020-12-03 | GSE162487 | GEO
Project description:MicroRNA expression profiling in human tumor cell lines treated with interferon-alpha-2a
| PRJNA116363 | ENA
Project description:We have previously shown that in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-elicited NAFLD progression, central carbon, glutaminolysis and serine/folate metabolism are reprogrammed to support NADPH production and ROS defenses. To further investigate underlying dose-dependent responses associated with TCDD-induced fibrosis, female C57BL/6 mice were gavaged with TCDD every 4 days (d) for 28d or 92d. RNA-Seq, ChIP-Seq (2hr), and 28d metabolomic (urine, serum, and hepatic extract) analyses were conducted with complementary serum marker assessments at 92d. Additional vehicle and 30 µg/kg treatment groups were allowed to recover for 36d following the 92d treatment regimen to examine recovery from TCDD-elicited fibrosis. Histopathology revealed dose-dependent increases in hepatic fat accumulation, inflammation, and periportal collagen deposition at 92d, with increased fibrotic severity in the recovery group. Serum proinflammatory and profibrotic interleukins-1β, -2, -4, -6, and -10, as well as TNFα and IFNγ, exhibited dose-dependent induction. An increase in glucose tolerance was observed with a concomitant 3.0-fold decrease in hepatic glycogen linked to increased ascorbic acid biosynthesis and proline metabolism, consistent with increased fibrosis. RNA-Seq identified differential expression of numerous matrisome genes including an 8.8-fold increase in Tgfb2 indicating myofibroblast activation. Further analysis suggests reprogramming of glycogen, ascorbic acid, and amino acid metabolism in support of collagen deposition and the use of proline as a substrate for ATP production via the proline cycle. Conclusion: In addition to metabolic reprogramming in support of NADPH production for ROS defense, we demonstrate that glycogen, ascorbic acid, and amino acid metabolism are also reorganized to support remodeling of the extracellular matrix, progressing to hepatic fibrosis in response to chronic injury from TCDD.
2016-09-01 | GSE81990 | GEO
Project description:Human tumor cell lines treated with interferon-alpha-2a
| PRJNA126607 | ENA
Project description:Expression data of interferon-alpha treated Huh-7 cells
| PRJNA148091 | ENA
Project description:Background: Clear guidelines for therapy of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) are missing due to the lack of randomized double-blind controlled clinical trials. Moderate yet similar clinical benefit has been demonstrated for IFN-a monotherapy and high-dose ascorbic acid (AA) monotherapy in open clinical trials. However, there is no clear evidence to support the value of one of these specific treatment approaches, due to the lack of in vivo and in vitro studies exploring and comparing the effects of high-dose AA and IFN-a treatment in the context of HAM/TSP. Principal Findings: Based on flow cytometry and thymidine incorporation, we demonstrated for the first time that high-dose AA displays superior antiproliferative and immunomodulatory effects over IFN-a in HAM/TSP PBMCs ex vivo. In addition, high-dose AA induces cell death in HTLV-1-infected T-cell lines in vitro. Microarray combined with Ingenuity Pathway Analysis revealed AA-induced modulation of genes associated with cell death and cell cycle. Conclusions: In comparison with IFN-a, high-dose AA is preferred as anti-HTLV-1 treatment in vitro, due to its superior cell death-inducing, antiproliferative and immunomodulatory effects. Considering the lack of treatment options, the mild in vivo side effects and the low cost price, high-dose AA should be further explored for its therapeutic potential in HAM/TSP treatment. In total, 15 samples were analyzed. One microarray experiment was performed, including triplicate samples for each treatment condition (untreated, IFN-a, 10 µg/ml ascorbic acid, 50 µg/ml ascorbic acid, 100 µg/ml ascorbic acid). Triplicate samples were obtained from three separate RNA experiments.
2012-06-13 | E-GEOD-34572 | biostudies-arrayexpress
Project description:Approximately 50% of patients with chronic hepatitis C (CHC) have a sustained virologic response (SVR) to treatment with pegylated interferon (pegINF)-α and ribavirin. Non-response to treatment is associated with constitutively increased expression of IFN-stimulated genes (ISGs) in the liver. Treatment of patients with acute hepatitis C (AHC) is more effective, with SVR rates >90%. We investigated mechanisms of the different responses of patients with CHC and AHC to pegIFN-α therapy. We analyzed IFN signaling and ISG expression in liver samples from patients with acute hepatitis C (AHC), patients with chronic hepatitis (CHC), and individuals without hepatitis C (controls) using microarray, immunohistochemical, and protein analyses. Findings were compared with those from primary human hepatocytes stimulated with IFN-α or IFN-γ, as reference sets. Expression levels of 100s of genes, primarily those regulated by IFN-γ, were altered in liver samples from patients with AHC compared with controls. Expression of IFN-γ–stimulated genes was induced in liver samples from patients with AHC, whereas expression of IFN-α–stimulated genes was induced in samples from patients with CHC. In an expression analysis of negative regulators of IFN-α signaling, we did not observe differences in expression of SOCS1 or SOCS3 between liver samples from patients with AHC and those with CHC. However, USP18 (another negative regulator of IFN-α signaling), was upregulated in liver samples of patients with CHC that did not respond to therapy, but not in AHC. In conclusion, differences in expression of ISGs might account for the greater response of patients with AHC, compared to those with CHC, to treatment with pegINF-α and ribavirin. Specifically, USP18 is upregulated in liver samples of patients with CHC that do not respond to therapy, but not in patients with AHC. (Interferon-γ Stimulated Genes, but not USP18, are Expressed in Livers of Patients with Acute Hepatitis C; Dill MT, Makowska Z et al, Gastroenterology 2012 (in press)) Primary human hepatocytes from 2 donors were analyzed. From each donor there are 5 samples: untreated cells, cells treated with interferon alpha (1000 IU/ml) for 6 and 24 hours and cells treated with interferon gamma (1000 IU/ml) for 6 and 24 hours.
2012-06-08 | E-GEOD-38147 | biostudies-arrayexpress
Project description:To investigate the effects of administration of carbon black nanoparticle (CB-NP) to pregnant mice on the brain development in infantile mice, we have employed whole-genome microarray expression profiling to identify genes which show dose-dependent differential expression with astrogliosis in the frontal cortex of offspring mice. Some pregnant mice were pretreated with ascorbic acid to investigate the mechanism underlying the CB-NP effect. In addition to the frontal cortex of offspring mice who were exposed to CB-NP maternally, placenta was also subjected to the analysis to investigate the mechanism. Pregnant mice were intranasally exposed to 0, 2.9, 15, 73, or 95 micro gram of CB-NP (Printex 90) per kg (body weight) on gestational days (GDs) 5 and 9. Some pregnant mice were treated with intraperitoneal injection of ascorbic acid (500 mg/kg) at 1 h before the CB-NP instillation (95 μg/kg). Placentae were collected from pregnant dams on GD 13. Dissected cerebral cortex were collected from 6- and 12-week-old offspring mice.
2023-12-20 | GSE250286 | GEO
Project description:Gene expression profiling of interferon-alpha-treated HTLV-1-infected CD4+ T cell lines
| PRJNA150111 | ENA