Proteome analysis of Beas-2B cells with S. pneumoniae D39
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Cell Culture
SUBMITTER: 
Kristin Surmann
LAB HEAD: Uwe Völker
PROVIDER: PXD039059 | Pride | 2023-07-04
REPOSITORIES: Pride
Dataset's files
Items per page: 5 1 - 5 of 71 |
Similar Datasets
Project description:Transcriptional profiling of primary monocyte derived macrophages (MDMs) comparing control untreated MDMs with MDMs exposed with Serotype 2 Streptococcus pneumoniae (D39) strain (MOI 10) for 3 hours) Three-condition experiment, control MDMs vs. D39 infected MDMs vs Stop infected MDMs. Biological replicates: 3 control replicates, 3 infected D39 replicates and 3 infected penumolysin deficient (STOP) MOI 10.
2021-03-01 | E-MTAB-9055 | biostudies-arrayexpress
Project description:The aim of the study was to identify differentially expressed genes during Gonadal Sex Determination in cattle. We performed a Rna-Seq analysis of XX and XY gonads during sex determination on embryonic days 35 (D35), 39 (D39) and 43 (D43). RNA-seq libraries were prepared from grouped gonads from D35, D39 and D43 males and females.
2019-08-30 | E-MTAB-7887 | biostudies-arrayexpress
Project description:We report the mRNA expression profile of Streptococcus pneumoniae Type 2 D39 strain-derived mutant lacking the phpP gene encoding eukaryote-type ser/thr phosphatase . Measuring transcriptome profiling in D39Î?phpP mutants vs D39-WT pneumococcus wild-type strain
2016-10-27 | E-GEOD-74421 | biostudies-arrayexpress
Project description:BackgroundHexavalent chromium [Cr(VI)] is a potent human carcinogen. Occupational exposure has been associated with increased risk of respiratory cancer. Multiple mechanisms have been shown to contribute to Cr(VI) induced carcinogenesis, including DNA damage, genomic instability, and epigenetic modulation, however, the molecular mechanism and downstream genes mediating chromium's carcinogenicity remain to be elucidated.Methods/resultsWe established chromate transformed cell lines by chronic exposure of normal human bronchial epithelial BEAS-2B cells to low doses of Cr(VI) followed by anchorage-independent growth. These transformed cell lines not only exhibited consistent morphological changes but also acquired altered and distinct gene expression patterns compared with normal BEAS-2B cells and control cell lines (untreated) that arose spontaneously in soft agar. Interestingly, the gene expression profiles of six Cr(VI) transformed cell lines were remarkably similar to each other yet differed significantly from that of either control cell lines or normal BEAS-2B cells. A total of 409 differentially expressed genes were identified in Cr(VI) transformed cells compared to control cells. Genes related to cell-to-cell junction were upregulated in all Cr(VI) transformed cells, while genes associated with the interaction between cells and their extracellular matrices were down-regulated. Additionally, expression of genes involved in cell proliferation and apoptosis were also changed.ConclusionThis study is the first to report gene expression profiling of Cr(VI) transformed cells. The gene expression changes across individual chromate exposed clones were remarkably similar to each other but differed significantly from the gene expression found in anchorage-independent clones that arose spontaneously. Our analysis identified many novel gene expression changes that may contribute to chromate induced cell transformation, and collectively this type of information will provide a better understanding of the mechanism underlying chromate carcinogenicity.
| S-EPMC3060877 | biostudies-literature
Project description:We report the differential expression of circRNAs between T-BEAS-2B cells (cadmium-transformed BEAS-2B cells) and C-BEAS-2B cells (passage-matched control BEAS-2B cells) by high-throughput sequencing. T-BEAS-2B cells are BEAS-2B cells transformed by cadmium at 2.0 μM for twenty weeks, and C-BEAS-2B cells are their passage-matched control. RNAs were sequenced on Illumina HiSeq Xten platform in triplicates, and expressions of circRNAs were calculated by TPM (transcripts per kilobase of exon model per million mapped reads). Clean data per sample exceeds 10 GB. We find 235 significantly up-regulated circRNAs and 271 significantly down-regulated circRNAs in T-BEAS-2B cells relative to C-BEAS-2B cells. Our work provides clues and evidence for exploring the mechanism of circRNAs in cadmium carcinogenesis.
2024-01-26 | GSE165549 | GEO
Project description:BEAS-2B was originally established as an immortalized but non-tumorigenic epithelial cell line from human bronchial epithelium. Because of general recognition for its bronchial epithelial origin, the BEAS-2B cell line has been widely used as an in vitro cell model in a large variety of studies associated with respiratory diseases including lung carcinogenesis. However, very few studies have discussed non-epithelial features of BEAS-2B cells, especially the features associated with mesenchymal stem cells (MSCs), which represent a group of fibroblast-like cells with limited self-renewal and differentiation potential to various cell lineages. In this study, we compared BEAS-2B with a human umbilical cord-derived MSCs (hMSCs) cell line, hMSC1, which served as a representative of hMSCs in terms of expressing common features of hMSCs. It was observed that both BEAS-2B and hMSC1 shared the same expression profile of surface markers of hMSCs and exhibited similar osteogenic and adipogenic differentiation potential. In addition, like hMSC1, the BEAS-2B cell line exhibited suppressive activities on proliferation of mitogen-activated total T lymphocytes as well as Th1 lymphocytes, and IFNγ-induced expression of IDO1, all thus demonstrating that BEAS-2B cells exhibited an almost identical characteristic profile with hMSCs, even though, there was a clear difference between BEAS-2B and hMSCs in the effects on type 2 macrophage polarization. Most importantly, the hMSCs features of BEAS-2B were unlikely a consequence of epithelial-mesenchymal transition. Therefore, this study provided a set of evidence to provoke reconsideration of epithelial origin of BEAS-2B.
| S-EPMC6941928 | biostudies-literature
Project description:BackgroundEosinophilic granulocytes are important for the human immune system. Many cationic proteins with cytotoxic activities, such as eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN), are released from activated eosinophils. ECP, with low RNase activity, is widely used as a biomarker for asthma. ECP inhibits cell viability and induces apoptosis to cells. However, the specific pathway underlying the mechanisms of ECP-induced cytotoxicity remains unclear. This study investigated ECP-induced apoptosis in bronchial epithelial BEAS-2B cells and elucidated the specific pathway during apoptosis.ResultsTo address the mechanisms involved in ECP-induced apoptosis in human BEAS-2B cells, investigation was carried out using chromatin condensation, cleavage of poly (ADP-ribose) polymerase (PARP), sub-G1 distribution in cell cycle, annexin V labeling, and general or specific caspase inhibitors. Caspase-8-dependent apoptosis was demonstrated by cleavage of caspase-8 after recombinant ECP treatment, accompanied with elevated level of tumor necrosis factor alpha (TNF-alpha). Moreover, ECP-induced apoptosis was effectively inhibited in the presence of neutralizing anti-TNF-alpha antibody.ConclusionIn conclusion, our results have demonstrated that ECP increased TNF-alpha production in BEAS-2B cells and triggered apoptosis by caspase-8 activation through mitochondria-independent pathway.
| S-EPMC2819994 | biostudies-literature
Project description:Nicotinamide riboside (NR), a NAD+ precursor, has received attention due to several health benefits it has induced in experimental models. Studies in cultured cells, animals, and humans consistently show increased NAD+ availability after NR supplementation, which is considered the only mode of NR action that leads to health benefits. In the present study, we show that a persistently low NR concentration (1 μM) in the growth medium of BEAS-2B human cells, grown in a monolayer, induces energy stress, which precedes a cellular NAD+ increase after 192 h. NR concentrations greater than 1 μM under the specified conditions were cytotoxic in the 2D cell culture model, while all concentrations tested in the 3D cell culture model (BEAS-2B cell spheroids exposed to 1, 5, 10, and 50 μM NR) induced apoptosis. Shotgun proteomics revealed that NR modulated the abundance of proteins, agreeing with the observed effects on cellular energy metabolism and cell growth or survival. Energy stress may activate pathways that lead to health benefits such as cancer prevention. Accordingly, the premalignant 1198 cell line was more sensitive to NR cytotoxicity than the phenotypically normal parent BEAS-2B cell line. The role of a mild energy stress induced by low concentrations of NR in its beneficial effects deserves further investigation. On the other hand, strategies to increase the bioavailability of NR require attention to toxic effects that may arise.
| S-EPMC11337214 | biostudies-literature
Project description:To profile the human substrate degradome of the SARS-CoV-2 main viral protease and to investigate whether 3CLpro cleavage of cellular substrates dampens host antiviral responses induced by type I interferons, we treated BEAS-2B cells with interferon-alpha (N = 3), interferon-beta (N = 3), or vehicle (N = 3), retrieve and exposed native proteome extracts from human embryonic kidney to 3CLpro cleavage. Then, N Terminal Amine Labeling of Substates (TAILS) was used to identify the substrates. Here, heavy [+34] isotope dimethyl labeling is performed at the whole protein level in the 3CLpro-exposed samples, and the P1' side of substrates substrates was revealed by comparing to the samples exposed to inactive mutant labeled with ligh [+28 Da] dimethyl.
2021-11-03 | PXD026815 | Pride
Project description:BEAS-2B cells are human bronchial epithelial cells, and often used as a in vitro model for the detection of potential pulmonary toxicity of chemicals. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes after treated with chemical substance
2017-01-10 | GSE93329 | GEO