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HeLa cells treated with V-ATPase inhibitors or with desoxyferramine compared to HeLa in DMSO or medium with low LDL

ABSTRACT: Expression data from HeLa cells treated with V-ATPase inhibitors or with desoxyferramine compared to HeLa treated with DMSO or medium with low LDL To determine which genes respond first to low concentrations of V-ATPase inhibition, we treated HeLa cells with two different V-ATPase inhibitors, bafilomycin and phenylsalicylihalamide (LX1077) at concentrations that slow cell growth by only 20%. To identify genes responding to expected effects of inhibiting the V-ATPase, expression data from inhibiting the V-ATPase was compared to that of chelating iron or incubating cells in medium with low LDL.

ORGANISM(S): Homo sapiens

PROVIDER: GSE16870 | GEO | 2010/07/22

SECONDARY ACCESSION(S): PRJNA117575

REPOSITORIES: GEO

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HeLa cells treated with V-ATPase inhibitors or with desoxyferramine compared to HeLa in DMSO or medium with low LDL

Project description:Expression data from HeLa cells treated with V-ATPase inhibitors or with desoxyferramine compared to HeLa treated with DMSO or medium with low LDL To determine which genes respond first to low concentrations of V-ATPase inhibition, we treated HeLa cells with two different V-ATPase inhibitors, bafilomycin and phenylsalicylihalamide (LX1077) at concentrations that slow cell growth by only 20%. To identify genes responding to expected effects of inhibiting the V-ATPase, expression data from inhibiting the V-ATPase was compared to that of chelating iron or incubating cells in medium with low LDL. We used microarrays to detail the global programme of gene expression in HeLa cells at 6, 12 & 24 hours culture in the presence of V-ATPase inhibitors. For each drug treatment, control cells were incubated at the same time with the same concentration of DMSO used as carrier for the drugs. HeLa cells were also treated with the iron chelator, desoxiferamine for 6 or 12 hours or with medium with low LDL for 12 hours to identify genes that respond to low iron or low cholesterol. Each timepoint and each treatment has two independent replicates. Experimental samples were compared to control samples grown on the same day.

2010-07-22 | E-GEOD-16870 | biostudies-arrayexpress

Homo sapiens

Project description:HeLa cells treated with V-ATPase inhibitors or with desoxyferramine compared to HeLa in DMSO or medium with low LDL

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Distinct signal transduction pathways downstream of the (P)RR revealed by microarray and ChIP-chip analyses [Expt: Geni_Bafi]

Project description:Within the overall project, we performed a set of microarray and chromatin-immunoprecipitation (ChIP)-chip experiments using siRNA against the (pro)renin receptor ((P)RR), stable overexpression of PLZF, the PLZF translocation inhibitor genistein and the specific V-ATPase inhibitor bafilomycin to dissect transcriptional pathways downstream of the (P)RR. In this dataset, we include the expression data obtained from KELLY cells incubated with genistein or bafilomycin A1. Five intervention samples and three control samples were analyzed. We generated the following pairwise comparisons using Chipinspector (Genomatix Software GmbH) and a FDR of 0.5% (bafilomycin), 5% (genistein): genistein- versus DMSO- and bafilomycin- versus DMSO-treated cells. ChipInspector carries out significance analysis on the single probe level. Normalized probe set level data not provided for individual Sample records. Processed data is available on Series record.

2013-07-05 | E-GEOD-39962 | biostudies-arrayexpress

Low LDL Cholesterol and Increased Risk of Type 2 Diabetes

Project description:<p>Lipid lowering therapy using HMG-CoA reductase inhibitors (statins) is associated with an approximately 9-12% increase in the risk of new-onset type 2 diabetes (T2DM). The risk of diabetes could be increased by statins directly; however, genetic approaches have also implicated low LDL cholesterol (LDL-C) concentrations as a risk factor for T2DM. Mendelian randomization studies using functional variants in both HMGCR (<a href="https://www.ncbi.nlm.nih.gov/gene/?term=HMGCR" target="_blank">GeneID:3156</a>) and PCSK9 (<a href="https://www.ncbi.nlm.nih.gov/gene/?term=PCSK9" target="_blank">GeneID:255738</a>) genes found a higher risk of T2DM in individuals with variants associated with lower LDL-C concentrations. Since PCSK9 and HMGCR are involved in lipid metabolism through distinct molecular pathways, the altered glycemic effect associated with variants in both genes is likely to be the result of their common effect on LDL-C concentrations.</p> <p>Despite the findings from statin clinical trials and genetic studies, there is little direct evidence implicating low LDL-C concentrations with increased risk of T2DM. Individuals who have very low LDL-C concentrations not due to lipid lowering therapy can provide insights into the relationship between low LDL-C concentrations and T2DM. Here, we used de-identified electronic health records (EHRs) to test the hypothesis that low LDL-C concentrations are associated with T2DM. </p>

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Spliceostatin treatment on HeLa cells

Project description:HeLa cell line treated with Spliceostatin or methanol

2011-03-08 | GSE22614 | GEO

RNA-Seq of HeLa cells

Project description:HeLa cells were treated with ActD and RNA sequenced to examine RNA stability

2022-03-10 | GSE198178 | GEO

Identification of coordinately regulated microRNA-gene networks that differ in baboons discordant for LDL-Cholesterol

Project description:Although the mechanisms underlying development of atherosclerosis are not well understood, LDL-C is known to influence expression of endothelial microRNAs (miRNAs) and gene-targets of miRNAs to promote cell senescence. However, the impact of LDL-C on expression of PBMC miRNAs and miRNA targeted genes in response to an atherogenic diet is not known. We hypothesized that miRNA expression profiles differ between baboons with low and high serum low-density lipoprotein cholesterol (LDL-C) concentrations in response to diet, and that microRNA-gene networks in baboons discordant for LDL-Cholesterol We generated small RNA libraries from baboons differing in their LDL-C response to dietary fat and cholesterol (low LDL-C, n = 3; high LDL-C, n = 3) using liver biopsies collected before and after a high-cholesterol, high-fat (HCHF) challenge diet. We sequenced the libraries using Next-Generation Illumina sequencing methods, analyzed the data using mirTools software and identified 517 baboon miRNAs: 490 homologous to human and 27 novel miRNAs. HCHF diet elicited expression of more miRNAs compared to baseline (chow) diet for both low and high LDL-C baboons. Seventeen miRNAs exhibited significant differential expression in response to HCHF diet in high LDL-C baboons compared to nine miRNAs in low LDL-C baboons. Putative miRNA targets were identified with TargetScan/Base tools. miRNAs significantly targeted more genes in high LDL-C baboons compared to low LDL-C responders. Further, we identified miRNA isomers and other non-coding RNAs that were differentially expressed in response to the challenge diet.Our discovery of differentially expressed baboon miRNAs and their targets is a fundamental step in understanding the role of non-coding RNAs in the modulation of dsylipidemia.

2019-03-20 | GSE114722 | GEO

Distinct signal transduction pathways downstream of the (P)RR revealed by microarray and ChIP-chip analyses [Expt: ChIP-chip]

Project description:We performed a set of microarray and chromatin-immunoprecipitation (ChIP)-chip experiments using siRNA against the (pro)renin receptor ((P)RR), stable overexpression of PLZF, the PLZF translocation inhibitor genistein and the specific V-ATPase inhibitor bafilomycin to dissect transcriptional pathways downstream of the (P)RR.

2013-07-05 | GSE39960 | GEO

Differential microRNA response to a high-cholesterol, high-fat diet in livers of low and high LDL-C baboons

Project description:Dysregulation of microRNAs (miRNAs) expression has been implicated in molecular genetics events leading to the progression and development of atherosclerosis. We hypothesized that miRNA expression profiles differ between baboons with low and high serum low-density lipoprotein cholesterol (LDL-C) concentrations in response to diet, and that a subset of these miRNAs regulate genes relevant to dyslipidemia and risk of atherosclerosis. We generated small RNA libraries from baboons differing in their LDL-C response to dietary fat and cholesterol (low LDL-C, n = 3; high LDL-C, n = 3) using liver biopsies collected before and after a high-cholesterol, high-fat (HCHF) challenge diet. We sequenced the libraries using Next-Generation Illumina sequencing methods, analyzed the data using mirTools software and identified 517 baboon miRNAs: 490 homologous to human and 27 novel miRNAs. HCHF diet elicited expression of more miRNAs compared to baseline (chow) diet for both low and high LDL-C baboons. Seventeen miRNAs exhibited significant differential expression in response to HCHF diet in high LDL-C baboons compared to nine miRNAs in low LDL-C baboons. Putative miRNA targets were identified with TargetScan/Base tools. miRNAs significantly targeted more genes in high LDL-C baboons compared to low LDL-C responders. Further, we identified miRNA isomers and other non-coding RNAs that were differentially expressed in response to the challenge diet.Our discovery of differentially expressed baboon miRNAs and their targets is a fundamental step in understanding the role of non-coding RNAs in the modulation of dsylipidemia.

2012-07-14 | E-GEOD-37249 | biostudies-arrayexpress

Effect of p38 SAPK activation on HeLa cells

Project description:HeLa cells were treated with 100 mM NaCl during 2h versus untreated. HeLa cells treated with 100 mM NaCl during 2h versus HeLa cells treated with 100 mM NaCl during 2h after pre-treatment with 10 μM SB203580 for 30 min. Alternative splicing is a crucial mechanism for gene regulation that is modulated in response to a wide range of extracellular stimuli. Stress-activated protein kinases (SAPKs) play a key role in controlling several steps of mRNA biogenesis. Here, we show that osmostress has a major impact on the regulation of alternative splicing (AS), which is partly mediated through the action of the p38 SAPK.

2019-04-16 | GSE117996 | GEO

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