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MEG3 Upregulation in Myotonic Dystrophy and Its Correction by Antisense Conjugates Targeting Disease-Causing Mutations [miRNA-seq]

ABSTRACT: MEG3 Upregulation in Myotonic Dystrophy and Its Correction by Antisense Conjugates Targeting Disease-Causing Mutations [miRNA-seq]

PROVIDER: PRJNA1090496 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28412828.fastq.gz	Fastqsanger.gz
	SRR28412829.fastq.gz	Fastqsanger.gz
	SRR28412830.fastq.gz	Fastqsanger.gz
	SRR28412831.fastq.gz	Fastqsanger.gz
	SRR28412832.fastq.gz	Fastqsanger.gz

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MEG3 Upregulation in Myotonic Dystrophy and Its Correction by Antisense Conjugates Targeting Disease-Causing Mutations [miRNA-seq]

Project description:MEG3 upregulation has been confirmed to independently promote apoptosis in cancer, cardiovascular disease, and Alzheimer’s Disease. In this study, we unveiled that MEG3 is highly upregulated in Myotonic Dystrophy 1 (DM1) human muscle cells when compared with wild type cells. It is also increased in the muscle of DM1 mouse models, 15-fold in HSA-LR, and 6-fold in LC15. We also observed an increase of MEG3 in SMA mice (5-fold) indicating that MEG3 levels could play a role in the neuromuscular pathology leading to cell loss. Additionally in DM1, RNA sequencing revealed transcript retention of miRNAs and LncRNAs in the nucleus versus the cytoplasm, a phenomenon not observed with mRNAs. This nuclear retention could exacerbate pathological mechanisms involving non-coding RNA, such as MEG3-led apoptosis. In DM1 mice (HSA-LR), the correction of DM1 pathology with a peptide antisense oligonucleotide conjugate targeting the repeat expansion, a family of compounds currently being tested in a DM1 clinical trial, was able to also reduce the levels of MEG3. When direct interventions for the root cause of a disease are unavailable, the downregulation of MEG3 and its effect on apoptosis may serve as an alternative therapeutic approach, notably in conditions that arise from complex interactions of genetic and environmental factors.

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MEG3 Upregulation in Myotonic Dystrophy and Its Correction by Antisense Conjugates Targeting Disease-Causing Mutations [mRNA-seq]

2025-03-21 | GSE262163 | GEO

MEG3 Upregulation in Myotonic Dystrophy and Its Correction by Antisense Conjugates Targeting Disease-Causing Mutations [mRNA-seq]

Project description:MEG3 Upregulation in Myotonic Dystrophy and Its Correction by Antisense Conjugates Targeting Disease-Causing Mutations [mRNA-seq]

| PRJNA1090497 | ENA

Antisense oligonucleotides targeting nuclear RNA for in vivo correction of myotonic dystrophy

Project description:This study examined the effects of antisense oligonucleotides (ASOs) on the muscle transcriptome in a transgenic mouse model of myotonic dystrophy. Two ASOs were tested in HSALR transgenic mice. Both of the ASOs targeted mRNA from a human skeletal actin (hACTA1) transgene. This transgene contains an expanded CTG repeat in the 3M-bM-^@M-^Y untranslated region (UTR) (Mankodi et al M-bM-^@M-^\Myotonic dystrophy in transgenic mice expressing an expanded CUG repeatM-bM-^@M-^] Science 2000; 289:1769-72). ASO 445235 targeted the hACTA1 transcript in the 3M-bM-^@M-^Y UTR, downstream from the expanded repeat. ASO 190401 targeted the hACTA1 transcript in the coding region. The HSALR mice received 4 weeks of biweekly subcutaneous injections of vehicle (saline), ASO 190401, or ASO 445236 (n = 4 per group), at a dose of 25 mg/kg per injection. Wild-type mice of the same strain background received saline injections (n = 4). One week after the final injection, quadriceps muscle was harvested for RNA analysis. Four conditions, four arrays per condition, to compare WT and HSALR trangenic mice without treatment (saline) and to examine the effect of two oligos (vs. saline) in the HSALR transgenic mice.

2012-06-27 | E-GEOD-38962 | biostudies-arrayexpress

Antisense oligonucleotides targeting nuclear RNA for in vivo correction of myotonic dystrophy

Project description:This study examined the effects of antisense oligonucleotides (ASOs) on the muscle transcriptome in a transgenic mouse model of myotonic dystrophy. Two ASOs were tested in HSALR transgenic mice. Both of the ASOs targeted mRNA from a human skeletal actin (hACTA1) transgene. This transgene contains an expanded CTG repeat in the 3’ untranslated region (UTR) (Mankodi et al “Myotonic dystrophy in transgenic mice expressing an expanded CUG repeat” Science 2000; 289:1769-72). ASO 445235 targeted the hACTA1 transcript in the 3’ UTR, downstream from the expanded repeat. ASO 190401 targeted the hACTA1 transcript in the coding region. The HSALR mice received 4 weeks of biweekly subcutaneous injections of vehicle (saline), ASO 190401, or ASO 445236 (n = 4 per group), at a dose of 25 mg/kg per injection. Wild-type mice of the same strain background received saline injections (n = 4). One week after the final injection, quadriceps muscle was harvested for RNA analysis.

2012-06-28 | GSE38962 | GEO

ChIP-seq in MEG3+ and MEG3- hIPSCs

Project description:In this experiment we sought to identify region with differential PRC2, JARID2, and H3K27me3 occupancy in human induced pluripotent stem cell lines with silenced or expressed MEG3 locus to indirectly determine the effect of this ncRNA on PRC2 function. 8 hIPSC lines, 5 MEG3+ and 3 MEG3-; ChIP-seq for EZH2, JARID2, and H3K27me3. Some done in replicates.

2013-12-25 | E-GEOD-48516 | biostudies-arrayexpress

Application of Antisense Conjugates for the Treatment of Myotonic Dystrophy Type 1.

Project description:Myotonic dystrophy type 1 (DM1) is one of the most common muscular dystrophies and can be potentially treated with antisense therapy decreasing mutant DMPK, targeting miRNAs or their binding sites or via a blocking mechanism for MBNL1 displacement from the repeats. Unconjugated antisense molecules are able to correct the disease phenotype in mouse models, but they show poor muscle penetration upon systemic delivery in DM1 patients. In order to overcome this challenge, research has focused on the improvement of the therapeutic window and biodistribution of antisense therapy using bioconjugation to lipids, cell penetrating peptides or antibodies. Antisense conjugates are able to induce the long-lasting correction of DM1 pathology at both molecular and functional levels and also efficiently penetrate hard-to-reach tissues such as cardiac muscle. Delivery to the CNS at clinically relevant levels remains challenging and the use of alternative administration routes may be necessary to ameliorate some of the symptoms experienced by DM1 patients. With several antisense therapies currently in clinical trials, the outlook for achieving a clinically approved treatment for patients has never looked more promising.

| S-EPMC9916419 | biostudies-literature

overexpression/knockdown MEG3 in C2C12 cell lines

Project description:MEG3 was known as a growth suppressor in tumor cells by activating p53. Besides, MEG3 could regulate transforming growth factor-β (TGF-β) signaling pathway, which is the key regulator of skeletal myogenesis and can enhance the proliferation of myogenic cells. Previous study also showed MEG3 was highly expressed in the paraxial mesoderm and probably regulated muscle development. To investigate the potential function of MEG3 in muscle development, we detected the expression levels of protein-coding genes after MEG3 over-expression or knockdown in C2C12 cell line using microarrays.

2018-09-28 | GSE73524 | GEO

Meg3 regulated genes in pancreatic beta cells

Project description:Meg3 is a long non-coding RNA. It's target genes are unknown. The mouse pancreatic beta cell line MIN6-4N was used to assess the expression of genes upon stable Meg3 overexpression Stable cell lines were isolated that have integated pcDNA3.1 or pcDNA3.1-mMeg3.The cells were processed for RNA isolation. The level of Meg3 expression was assessed by RT-PCR. RNA preps were used for microarray analysis.

2015-05-21 | E-GEOD-57716 | biostudies-arrayexpress

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Project description:This experiment was designed to detect differences in PRC2 occupancy in a human induced pluripotent cell line (MRC5) naturally deficient in MEG3 RNA after lentiviral overexpression of MEG3. MRC5 were transduced with lentiviruses for the overexpression of MEG3 lncRNA or GFP as a control. ChIP-seq was performed with EZH2 and JARID2 antibodies.

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