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Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair [RNA-seq]

ABSTRACT: Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair [RNA-seq]

PROVIDER: PRJNA974475 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24673481_1.fastq.gz	Fastqsanger.gz
	SRR24673481_2.fastq.gz	Fastqsanger.gz
	SRR24673482_1.fastq.gz	Fastqsanger.gz
	SRR24673482_2.fastq.gz	Fastqsanger.gz
	SRR24673483_1.fastq.gz	Fastqsanger.gz

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Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair

Project description:Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair

| PRJNA974473 | ENA

Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair [HiChIP]

Project description:Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair [HiChIP]

| PRJNA974477 | ENA

Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair [Cut&Run]

Project description:Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair [Cut&Run]

| PRJNA974476 | ENA

Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair [HiChIP]

Project description:Failure of oligodendrocytes to remyelinate underlies diseases such as multiple sclerosis (MS). We found that epigenetic silencing prevents oligodendrocytes from producing myelin sheaths in demyelinating MS lesions. Here, we developed a transgenic reporter system to identify a small-molecule epigenetic modulator that stimulates oligodendrocyte maturation and myelin ensheathment in vitro. This compound promoted remyelination in animal models of MS and myelination of regenerated axons and increased myelin sheath lengths in human iPSC-derived organoids. Multi-omics analyses revealed that the compound induced an enhancer/super-enhancer landscape that upregulates crucial myelinogenesis-associated pathways, including RRAS2-AKT signaling, driving actin depolymerization necessary for myelin ensheathment. Strikingly, the compound also induced phase-separated nuclear condensates of SREBP1/2, which concentrate transcriptional co-activators to drive lipid and cholesterol biosynthesis. Silencing expression of a potential target of the small molecule, HDAC3, facilitated robust myelination and remyelination. Our findings suggest that small-molecule-modulated epigenome rejuvenation relieves epigenetic silencing barriers and promotes myelin repair.

2024-05-24 | GSE232954 | GEO

Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair [RNA-seq]

2024-05-24 | GSE232955 | GEO

Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair [Cut&Run]

2024-05-24 | GSE232953 | GEO

Small-molecule-induced epigenetic rejuvenation overcomes myelinogenic barriers and stimulates myelin repair

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-24 | GSE232956 | GEO

A Histone Deacetylase 3-Dependent Pathway Delimits Peripheral Myelin Growth and Functional Regeneration [ChIP-Seq]

Project description:Schwann cell remyelination defects impair functional restoration after nerve damage, contributing to peripheral neuropathies. The mechanisms that mediate remyelination block remain elusive. Upon small-molecule epigenetic screening, we identified HDAC3, a histone-modifying enzyme, as a potent inhibitor of peripheral myelinogenesis. Inhibition of HDAC3 markedly enhances myelin growth and regeneration, and improves functional recovery after peripheral nerve injury. HDAC3 antagonizes myelinogenic neuregulin/PI3K/AKT signaling axis. Moreover, genome-wide profiling analyses reveal that HDAC3 represses pro-myelinating programs through epigenetic silencing, while coordinating with p300 histone acetyltransferase to activate myelination-inhibitory programs that include HIPPO signaling effector TEAD4 to inhibit myelin growth. Schwann-cell-specific deletion of either Hdac3 or Tead4 results in a profound increase in myelin thickness in sciatic nerves. Thus, our findings identify the HDAC3-TEAD4 network as a dual-function switch of cell-intrinsic inhibitory machinery that counters myelinogenic signals and maintains peripheral myelin homeostasis, highlighting the therapeutic potential of transient HDAC3 inhibition for improving peripheral myelin repair.

2018-02-11 | GSE93160 | GEO

A Histone Deacetylase 3-Dependent Pathway Delimits Peripheral Myelin Growth and Functional Regeneration [RNA-seq]

2018-02-11 | GSE93159 | GEO

Development of gene expression signatures for identifying novel factors that can overcome age-associated reprogramming barriers

Project description:To investigate the molecular features underlying senescence and rejuvenation during aged cell reprogramming and identify novel factors that can overcome age-associated barriers, we compared gene expression for reprogramming intermediates on D8 of tail-tip fibroblasts (TTFs) from young Wild Type (WT), old WT, and old p16 knockout (KO) mice. We collected TTFs from young WT, old WT, and old p16 KO mice and reprogrammed the cells by introducing four reprogramming factors, including Oct4, Sox2, Klf4, and c-Myc. Gene expression of reprogramming intermediates on D8 were compared. Two independent experiments were performed using different mice donors for each experiment.

2016-03-31 | E-GEOD-79747 | biostudies-arrayexpress

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