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HF liver: Control vs. Plin2-ASO treated

ABSTRACT: Transcriptional profiling of mouse liver comparing control, scrambled-oligonucleotides (Cont)-treated mice with Perilipin 2-antisense oligonucleotides (Plin2-ASO)-treated mice. C57BL/6 mice on a high-fat diet were treated with oligonucleotides in vivo. The goal was to determine the effects of Plin2 down-regulation in the liver on global gene expression. Two-condition experiment, control oligonucleotides vs. Plin2-antisense oligonucleotides. Biological replicates: 4 control replicates, 4 Plin2-ASO replicates.

ORGANISM(S): Mus musculus

SUBMITTER: yumi imai

PROVIDER: E-GEOD-37011 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Effects of perilipin 2 antisense oligonucleotide treatment on hepatic lipid metabolism and gene expression.

Imai Yumi Y Boyle Siobhan S Varela Gladys M GM Caron Emilie E Yin Xiaoyan X Dhir Raina R Dhir Ravindra R Graham Mark J MJ Ahima Rexford S RS

Physiological genomics 20120925 22

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide. We previously showed that Perilipin 2 (Plin2), a member of lipid droplet protein family, is markedly increased in fatty liver, and its reduction in the liver of diet-induced obese mice by antisense oligonucleotide (ASO) decreased steatosis and enhanced insulin sensitivity. Plin2-ASO treatment markedly suppressed lipogenic gene expression. To gain a better understanding of the biological role of Plin2 in liver, w ...[more]

PMID: 23012396

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HF liver: Control vs. Plin2-ASO treated

Project description:Transcriptional profiling of mouse liver comparing control, scrambled-oligonucleotides (Cont)-treated mice with Perilipin 2-antisense oligonucleotides (Plin2-ASO)-treated mice. C57BL/6 mice on a high-fat diet were treated with oligonucleotides in vivo. The goal was to determine the effects of Plin2 down-regulation in the liver on global gene expression.

2012-12-05 | GSE37011 | GEO

HIPSTR lncRNA knockdown in HEK293 cells

Project description:HIPSTR is a conserved lncRNA that is transcribed antisense to TFAP2A gene. Unlike previously reported antisense lncRNAs, HIPSTR expression does not correlate with the expression of its antisense counterpart. HIPSTR depletion in HEK293 and H1BP cells predominantly affects genes involved in early organismal development and cell differentiation. HEK293 cells were transfected with antisense oligonucleotides (ASOs) targeting HIPSTR (ASO #1 or ASO #2) or control scrambled ASO (ASO CTL); transfection with each ASO was done in triplicate.

2016-09-08 | E-GEOD-77935 | biostudies-arrayexpress

HIPSTR lncRNA knockdown in H1BP cells

Project description:HIPSTR is a conserved lncRNA that is transcribed antisense to TFAP2A gene. Unlike previously reported antisense lncRNAs, HIPSTR expression does not correlate with the expression of its antisense counterpart. HIPSTR depletion in HEK293 and H1BP cells predominantly affects genes involved in early organismal development and cell differentiation. H1BP cells were transfected with antisense oligonucleotides (ASOs) targeting HIPSTR (ASO #0, ASO #1 or ASO #2) or control scrambled ASO (ASO CTL); transfections with each targeting ASO were done in duplicate, transfections with control ASO were done in triplicate.

2016-09-08 | E-GEOD-77936 | biostudies-arrayexpress

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Project description:Human FOXP3 antisense oligonucleotides (ASOs) target effects in primary iTregs gene expression. Tregs were isolated from human PBMCs from 5 different donors, subjected to one of 4 different treatments: (1) Untreated, (2) Control ASO 792169, (3) FOXP3 ASO 910959, (4) FOXP3 ASO 910956 under either stimulation with aCD3/aCD28 coated beads or left unstimulated.

2024-01-08 | E-MTAB-11589 | biostudies-arrayexpress

Inhibiting Monoacylglycerol Acyltransferase 1 Ameliorates Hepatic Metabolic Abnormalities, but not Inflammation and Injury in Mice

Project description:Abnormalities in hepatic lipid metabolism are believed to play a critical role in the etiology of nonalcoholic steatohepatitis (NASH). Monoacylglycerol acyltransferase (MGAT) enzymes convert monoacylglycerol to diacylglycerol, which is the penultimate step in one pathway for triacylglycerol (TAG) synthesis. Hepatic expression of Mogat1, which encodes an MGAT enzyme, is increased in the livers of mice with hepatic steatosis and knocking down Mogat1 improves insulin sensitivity, but whether increased MGAT activity plays a role in the etiology of NASH is unclear. To examine the effects of knocking down Mogat1 in the liver on the development of NASH, C57BL/6 mice were placed on a diet containing high levels of trans fatty acids, fructose, and cholesterol (HTF-C diet) or a low fat control diet for 4 weeks. Mice were then injected with antisense oligonucleotides (ASO) to knockdown Mogat1 or a scrambled ASO control for 12 weeks while remaining on diet. HTF-C diet caused glucose intolerance, hepatic steatosis, and induced hepatic gene expression markers of inflammation, macrophage infiltration, and stellate cell activation. Mogat1 ASO treatment, which suppressed Mogat1 expression in liver, attenuated weight gain, improved glucose tolerance, and decreased hepatic TAG content compared to control ASO-treated mice on HTF-C chow. However, Mogat1 ASO treatment did not reduce hepatic DAG, cholesterol, or free fatty acid content, improve histologic measures of liver injury, or reduce expression of markers of stellate cell activation, liver inflammation, and injury. In conclusion, inhibition of hepatic Mogat1 in HTF-C diet-fed mice improves glucose tolerance and hepatic TAG accumulation without attenuating liver inflammation and injury. Total RNA obtained from liver of 4 control vs. 4 Mogat1 ASO treated higf-fat diet (HFD) fed mice.

2014-11-05 | E-GEOD-60349 | biostudies-arrayexpress

Preliminary small RNAseq of human breast cancer cell line MDA-MB-231 transfected with antisense oligonucleotide 1537S (ASO-1537S), compared to control oligonucleotide (ASO-C) and untreated cells

Project description:Proliferation of tumor cells transfected with ASO-1537S is inhibited compared to controls. The aim of the experiment is to determine changes in microRNA expression profiles with treatment, compared to controls.

2023-06-02 | E-MTAB-6762 | biostudies-arrayexpress

Small RNAseq of human breast cancer cell line MDA-MB-231 transfected with antisense oligonucleotide 1537S (ASO-1537S), compared to control oligonucleotide (ASO-C) and untreated cells

2023-06-02 | E-MTAB-6768 | biostudies-arrayexpress

Fip1 iCLIP-seq in Hela cells without treatment or treated with negative control anti-sense oligos (ASO) or snoRD50a ASO to study how snoRD50a affects Fip1/RNA interaction in mRNA 3' processing

Project description:We aimed to discover trans-acting RNA molecules involved in mRNA 3 processing. We reasoned that, if there exist such functional RNAs, they must directly associate with the key machinery responsible for mRNA 3 processing. Therefore, it would be of great value to comprehensively identify RNAs interacting with pre-mRNA 3 processing complex. To this goal, we took advantage of previously well-characterized system combined with high-throughput sequencing to investigate the target RNAs at the transcriptomic level. Fip1 protein is an essential mRNA 3' processing factor. Our in vitro data suggested that snoRD50a affects Fip1/RNA interaction in SV40 late (SVL) polyA site 3' processing. To determine whether snoRD50a influences Fip1/RNA interaction at transcriptomic level in vitro, we performed Fip1 iCLIP-seq experiments in Hela cells transfected with control NC ASO (negative control anti-sense DNA) or snoRD50a ASO.

2017-06-01 | E-MTAB-5384 | biostudies-arrayexpress

Gapmer ASO targeting

Project description:Antisense oligonucleotides gapmers with multiple targets

| PRJEB53196 | ENA

Searching for human genes whose expression is controlled by nuclear paraspeckle

Project description:To identify human genes whose expression is controled by nuclear paraspeckle, the microarray was carried out using the RNA samples prepared from the control and NEAT1 lncRNA knockdown HeLa cells where the nucelar paraspckels were disintegrated. NEAT1 lncRNA was eliminated by administration of antisense oligogapmer. Either NEAT1 ASO (#12) or control ASO (GFP) was ademnistered into HeLa cells to knockdown NEAT1 lncRNA. Total RNAs were prepared after 6, 12 and 24 hours after ASO administration.

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