Identification of genes involved in apoptosis-induced by cold atmospheric pressure plasma in human lymphoma U937 cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE76022 | GEO | 2015/12/15
SECONDARY ACCESSION(S): PRJNA306024
REPOSITORIES: GEO
Similar Datasets
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
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Project description:Legumes establish symbiosis with soil rhizobia forming root nodules that fix atmospheric nitrogen. The central role of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in nodule biology has been clearly established. Recently, hydrogen sulfide (H2S) and other reactive sulfur species (RSS) have emerged as novel signaling molecules in animals and plants. A major mechanism by which ROS, RNS, and RSS fulfil their signaling role is the post-translational modification of proteins. To identify possible functions of H2S in nodule development and senescence, we used the tag-switch method to analyze quantitative changes in the persulfidation profile of common bean (Phaseolus vulgaris) nodules at different developmental stages. The proteomic analysis suggests that persulfidation plays a major regulatory role in plant and bacteroid metabolism and senescence. In addition, the effect of a H2S donor on several proteins involved in ROS and RNS homeostasis was investigated. The results obtained using nodule extracts and recombinant proteins suggest a crosstalk between H2S, ROS, and RNS, and a protective function of persulfidation on redox-sensitive enzymes from oxidative modifications that may cause enzyme inactivation. It is concluded that the general decrease of persulfidation levels observed in plant proteins of aging nodules is one of the mechanisms that cause the disruption of redox homeostasis leading to senescence.
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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
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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).
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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: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
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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
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