Identification of genes involved in apoptosis-induced by cold atmospheric pressure plasma in human lymphoma U937 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE76022 | GEO | 2015/12/15
SECONDARY ACCESSION(S): PRJNA306024
REPOSITORIES: GEO
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Project description:Cold atmospheric pressure plasma (CAP) is known as a source of biologically active agents, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS). Recent medical investigations have focused on applying CAP to cancer treatment. There is also growing evidence that exposure of cells to CAP or CAP-activated medium induces apoptosis in cancer cells, and ROS and/or RNS are considered to be effective agents to CAP-induced apoptosis. More recently, we demonstrated that Ar-CAP or Ar containing 2.5 % of N2 (Ar-N2-CAP) significantly induced apoptosis in human lymphoma U937 cells. However, a detailed molecular mechanism underling the induction of apoptosis by CAP in cancer cells is unclear. In the present study, to identify genes involved in the induction of apoptosis by CAP in human lymphoma U937 cells, global-scale gene expression analysis was performed using a GeneChip® system. Human lymphoma U937 cells were treated with Ar-CAP or Ar-N2-CAP. Total RNA samples were prepared from the cells, and quality of the RNA was analyzed using a Bioanalyzer 2100. Gene expression was analyzed by an Affymetrix GeneChip® system with a Human Genome U133-plus 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturerâs instructions.
2015-12-15 | E-GEOD-76022 | biostudies-arrayexpress
Project description:Here, we investigated the role of mononuclear phagocytes associated nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX-2) in inflammatory neurodegeneration. Cybb-deficient mice NOX-2 knock-out (KO) and control wild type (WT) mice were treated intraperitoneally daily over four consecutive days with 1 µg/gbw/day LPS. Repeated LPS injections led to inflammation and neuronal loss in the brains of WT mice, which was attenuated after knockout of NOX-2. Transcriptome analysis by RNA-seq of total brain tissue indicated increased LPS-induced upregulation of genes belonging to the reactive oxygen species (ROS) and reactive nitrogen species (RNS) production, complement and lysosome activation as well as apoptosis and necroptosis in WT compared to NOX-2 KO mice.
2020-08-03 | GSE153369 | GEO
Project description:Nitric oxide and NO-derived species (RNS) are defense molecules with broad antimicrobial activity. Micro-organisms have developed strategies to sense RNS and counteract their damaging effects. We used Saccharomyces cerevisiae, harbouring a deletion of YHB1 that encodes the main NO scavenger enzyme, to study consequences of RNS exposure on whole genome transcriptional response. The expression of >700 genes was altered on RNS treatment. No major role for ROS-scavenging enzymes was found, and the respiratory chain, the main site of ROS production, had only minor involvement in the RNS-induced stress. The changes were generally transient and also found after treatment with the respiratory inhibitor myxothiazol. 117 genes however showed a persistent response which was not observed after myxothiazol treatment. Of these, genes of the glutathione and DNA repair systems, iron homeostasis and transport were found up-regulated. Severe repression of genes of respiratory chain enzymes was observed. Many of these genes are known to be regulated by the transcription factor Hap1p suggesting that RNS might interfere with Hap1p activity. We showed also that Msn2/4p and Yap1p, key regulators of the response to, respectively, general stress and oxidative stress, played a role in mediating the RNS-induced response.
2006-03-02 | E-MEXP-580 | biostudies-arrayexpress
Project description:Here, the effects of non-thermal low intensity pulsed ultrasound (LIPUS) on the gene expression in human lymphoma U937 cells were investigated using by an Affymetrix GeneChip system. Six hours after LIPUS treatment (0.3 W/cm2 for 1 min), apoptosis (14±3.8%, mean±SD) with minimal cell lysis was observed. At 3 h post-treatment, LIPUS down-regulated 193 genes and up-regulated 201 genes by >1.5-fold. Keywords: ultrasound, gene expression, Human lymphoma U937 cell
2008-01-23 | GSE10212 | GEO
Project description:Anisomycin is known as a potent apoptosis inducer by activating JNK/SAPK and inhibiting protein synthesis during translation. However, only few details are known on the mechanism of apoptosis induced by this compound. Genes in apoptosis induced by anisomycin in human leukemia U937 cells were investigated by using an Affymetrix GeneChip system. DNA fragmentation and phosphatidylserine externalization assays clearly demonstrated that anisomycin induced apoptosis in a time- and concentration- dependent manner. Of 22,283 probe sets analyzed, this compound down-regulated 524 probe sets and up-regulated 523 by a factor 1.5 or greater. Keywords: anisomycin, gene expression, Human lymphoma U937 cell
2007-06-23 | GSE8229 | GEO
Project description:Reactive nitrogen species (RNS) derived from dietary and salivary inorganic nitrates (NO3-) foment innate host defenses associated with the acidity of the stomach. The mechanisms by which these reactive species exert antibiotic activity in the gastric lumen are, however, poorly understood. To identify targets of RNS, the genetically tractable acid tolerance response (ATR) that enables enteropathogens to survive the harsh acidity of the stomach was screened for signaling pathways responsive to RNS. The nitric oxide (NO) donor spermine NONOate derepressed the Fur regulon that controls secondary lines of resistance against organic acids. Despite inducing a Fur-mediated adaptive response, acidified RNS largely boosted gastric host defenses as demonstrated by the fact that Salmonella bacteria exposed to spermine NONOate during mildly acidic conditions were not only shed in low amounts in feces, but also exhibited ameliorated oral virulence. NO prevented Salmonella from mounting a de novo ATR, but was unable to suppress an already functional protective response, indicating that RNS target regulatory cascades but not the effectors that defend against the rigors of gastric acidity. Transcriptional and translational analyses revealed that the PhoPQ signaling cascade is a critical ATR target of NO in rapidly growing Salmonella. Inhibition of PhoPQ signaling appears to contribute to most of the NO-mediated abrogation of the ATR in log phase bacteria, because the augmented acid sensitivity of phoQ-deficient Salmonella was not further enhanced after RNS treatment. Since PhoPQ-regulated acid resistance is widespread in enteric pathogens, the RNS-mediated inhibition of the Salmonella ATR described herein may represent a common component of the innate host defenses of the gastric lumen. Keywords: acid tolerance response, nitric oxide Microarray analyses were conducted comparing transcript levels of log-phase Salmonella cultured in minimal E salts + 0.4% glucose, pH 4.4 in the presence or absence of 250 µM spermine NONOate for 1 hour. Microarrays were performed in triplicate under identical conditions (3 biological replicates).
2010-05-26 | E-GEOD-9398 | biostudies-arrayexpress
Project description:The fungi of Paracoccidioides spp. genus are the causative agents of paracoccidioidomycosis (PCM), a systemic mycosis endemic to Latin America. This fungus is considered a facultative intracellular pathogen that is able to survive and replicate inside macrophages. The survival of the fungus during infection depends on its adaptability to various conditions, such as nitrosative/oxidative stress produced by the host immune cells, particularly alveolar macrophages. Currently, there is little knowledge about the P. brasiliensis signaling pathways involved in the fungus evasion mechanism of the host defense response. However, it is known that some of these pathways are triggered by reactive oxygen species and reactive nitrogen species (ROS/RNS) produced by host cells. Considering that the effects of NO (nitric oxide) on pathogens are concentration dependent, such effects could alter the redox state of cysteine residues by influencing (activating or inhibiting) a variety of protein functions, notably S-nitrosylation, a highly important NO-dependent posttranslational modification that regulates cellular functions and signaling pathways. It has been demonstrated by our group that P. brasiliensis yeast cells proliferate when exposed to low NO concentrations. Thus, this work investigated the modulation profile of S-nitrosylated proteins of P. brasiliensis, as well as identifying S-nitrosylation sites after treatment with RNS. Through mass spectrometry analysis (LC-MS/MS) and label-free quantification, it was possible to identify 474 proteins in the S-nitrosylated proteome study. With this approach, we observed that proteins treated with NO at low concentrations presented a proliferative response pattern, with several proteins involved in cellular cycle regulation and growth being activated. These proteins appear to play important roles in fungal virulence. On the other hand, proteins stimulated by high NO concentrations exhibited a survival response pattern, which may help to elucidate RNS antifungal properties and identify potential molecular targets for the development of new drugs in the future
2020-06-28 | PXD018775 | Pride
Project description:A series of trinucleotide cap analogs functionalized with an amine-terminated linker at the guanosine ribose and immobilized on BrCN-activated Sepharose was prepared. These affinity resins AR-1 (Am), AR-2 (m6Am), and AR-3 (Bn6Am) were incubated with HEK293F cell extract in the presence of GTP to limit non-specific interactions. The pulled-down proteins were eluted with the corresponding trinucleotide cap analog (m7GpppAmpG for AR-1, m7Gpppm6AmpG for AR-2, and m7GpppBn6AmpG for AR-3), digested with trypsin, labeled with isobaric tags (TMT), and analyzed by shotgun proteomics. This experiment was performed in order to assess binding preferences of proteins to the resins AR-1, AR-2, and AR-3.
2024-03-08 | PXD046838 | Pride
Project description:Production of reactive oxygen species (ROS) is one of the important antimicrobial mechanisms of phagocytic cells. Enhanced oxidative burst requires these cells to be primed with agents such as IFNg and LPS with a synergistic effect of these agents on the level of the burst. However, excessive ROS generation will lead to tissue damage and has been implicated in a variety of inflammatory and autoimmune disease. Therefore, this process needs to be tightly regulated. In order to understand the genes regulating this process, we will treat bone marrow derived macrophages with above mentioned priming agents and study the gene expression. We used microarrays to determine the changes in gene expression that occur in bone marrow derived macrophages after treatment with IFNg, LPS, or a combination of IFNg and LPS. Four condition experiment; Biological replicates: four replicates per condition
2014-03-31 | E-GEOD-53986 | biostudies-arrayexpress
Project description:Reactive nitrogen species (RNS) derived from dietary and salivary inorganic nitrates (NO3-) foment innate host defenses associated with the acidity of the stomach. The mechanisms by which these reactive species exert antibiotic activity in the gastric lumen are, however, poorly understood. To identify targets of RNS, the genetically tractable acid tolerance response (ATR) that enables enteropathogens to survive the harsh acidity of the stomach was screened for signaling pathways responsive to RNS. The nitric oxide (NO) donor spermine NONOate derepressed the Fur regulon that controls secondary lines of resistance against organic acids. Despite inducing a Fur-mediated adaptive response, acidified RNS largely boosted gastric host defenses as demonstrated by the fact that Salmonella bacteria exposed to spermine NONOate during mildly acidic conditions were not only shed in low amounts in feces, but also exhibited ameliorated oral virulence. NO prevented Salmonella from mounting a de novo ATR, but was unable to suppress an already functional protective response, indicating that RNS target regulatory cascades but not the effectors that defend against the rigors of gastric acidity. Transcriptional and translational analyses revealed that the PhoPQ signaling cascade is a critical ATR target of NO in rapidly growing Salmonella. Inhibition of PhoPQ signaling appears to contribute to most of the NO-mediated abrogation of the ATR in log phase bacteria, because the augmented acid sensitivity of phoQ-deficient Salmonella was not further enhanced after RNS treatment. Since PhoPQ-regulated acid resistance is widespread in enteric pathogens, the RNS-mediated inhibition of the Salmonella ATR described herein may represent a common component of the innate host defenses of the gastric lumen. Keywords: acid tolerance response, nitric oxide
2008-03-01 | GSE9398 | GEO