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Searching for human genes whose expression is controlled by nuclear paraspeckle

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Tetsuro Hirose

PROVIDER: E-GEOD-45158 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2013-03-15 | GSE45158 | 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

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

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. Two-condition experiment, control oligonucleotides vs. Plin2-antisense oligonucleotides. Biological replicates: 4 control replicates, 4 Plin2-ASO replicates.

2012-12-05 | E-GEOD-37011 | biostudies-arrayexpress

Noncoding RNAs induce TDP43 pathology in the ALS-iPSC models

Project description:Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron (MN) degenerative disease with a major pathological feature of cytoplasmic TDP-43 aggregation. However, the mechanisms underlying TDP-43 proteinopathy are still largely unknown. We performed in vitro differentiation of ALS-induced pluripotent stem cells (ALS-iPSCs; carrying the TDP-43M337V mutation) and isogenic controls and found upregulation of paraspeckle-associated lncRNA NEAT1 isoforms in the ALS-iPSC-derived MNs (ALS-iPSC-MNs). Intriguingly, the upregulated NEAT1 isoforms were mislocalized to the cytoplasm of ALS-iPSC-MNs, and the cytoplasmic NEAT1 provoked TDP-43 and TDP-43M337V liquid-liquid phase separation, generating long-lived protein condensates. These condensates had reduced mobility and were converted into aggregates, finally co-aggregating with phospho-TDP-43. Disruption of NEAT1 expression reduced its cytoplasmic levels and also reduced the levels of TDP-43/TDP-43M337V condensates. In 3D neuromuscular organoids with the TDP-43M337V mutation, treatment with NEAT1-antisense oligonucleotides (NEAT1-ASO) promoted neuromuscular junction formation and function, as well as muscle contractility. Furthermore, treatment of TDP-43Q331K mice with Neat1-ASO attenuated TDP-43 pathology in spinal cord and preserved motor function. These findings suggest that NEAT1 plays an important role in TDP-43-associated pathology, and NEAT1-ASO may attenuate pathological TDP-43 aggregation to prevent motor neuron degeneration and muscle weakness in ALS.

2024-11-24 | GSE189470 | GEO

Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for amyotrophic lateral sclerosis and frontotemporal dementia (strand specific RNA-seq)

Project description:Purpose: The purpose of this experiment is to identify expression changes after ASO-dependent depletion of mouse C9orf72 in the spinal cord of wild-type C57Bl/6 female mice. Methods: Strand specific RNA-seq was performed using RNAs extracted from spinal cord of C57Bl/6 mice two weeks after intracerebroventricular stereotactic injection of saline (n=3), a control ASO (n=3) or an ASO targeting mouse C9orf72 (n=3). C9orf72 RNA levels were reduced to approximately 30% of control levels in spinal cords from mice treated with the C9orf72 ASO. Results: Statistical comparison of RPKM values between RNAs from C9orf72 and control ASO treated animals or C9orf72 and saline treated samples revealed that only 12 genes were consistently upregulated (defined by P<0.05 adjusted for multiple testing) and 12 genes including C9orf72 were downregulated (defined by P<0.05 adjusted for multiple testing). Conclusions: Only few RNA expression changes were identified in the spinal cord following reduction of C9orf72. Use of strand specific RNA-seq to test the consequences of C9orf72 loss of function in mouse spinal cord.

2013-11-12 | E-GEOD-51685 | biostudies-arrayexpress

In vitro FOXP3 knockdown in human PBMCs

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

Expression data from NEAT1 regulated genes with or without polyI:C

Project description:Although thousands of long non-coding RNAs (lncRNAs) are localized in the nucleus, only a few dozen have been functionally characterized. We found that nuclear paraspeckle assembly transcript 1 (NEAT1), an essential lncRNA for the formation of nuclear body paraspeckles, is induced by poly I:C stimulation, resulting in excess formation of paraspeckles. Using microarray analysis, we investigated whether NEAT1 induction followed by excess formation of paraspeckles was involved in poly I:C-inducible gene expression. We want to know the NEAT1-regulated genes. To the end, HeLa TO cells with and without poly I:C stimulation and NEAT1-knock down cells with and without poly I:C stimulation and cells transfected with mock plasmid or Neat1v2 expression plasmid alone were used for RNA extraction and hybridization on Affymetrix microarrays.

2014-05-07 | E-GEOD-56936 | biostudies-arrayexpress

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