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RNA-sequence facilitates analyze changes of signaling pathways after cell reprogramming

ABSTRACT: RNA-sequence facilitates analyze changes of signaling pathways after cell reprogramming

PROVIDER: PRJNA1018964 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26113222_1.fastq.gz	Fastqsanger.gz
	SRR26113222_2.fastq.gz	Fastqsanger.gz
	SRR26113223_1.fastq.gz	Fastqsanger.gz
	SRR26113223_2.fastq.gz	Fastqsanger.gz
	SRR26113224_1.fastq.gz	Fastqsanger.gz

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RNA-sequence facilitates analyze changes of signaling pathways after drug treatment

Project description:RNA-sequence facilitates analyze changes of signaling pathways after drug treatment

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RNA-sequence facilitates analyze changes of signaling pathways after cell reprogramming

Project description:Cochlear hair cells are the sensory cells responsible for transduction of acoustic signals. In mammals, damaged hair cells do not regenerate, resulting in permanent hearing loss. Reprogramming of the surrounding supporting cells to functional hair cells represent a novel strategy to hearing restoration. However, cellular processes governing the efficient and functional hair cell reprogramming are not completely understood. Employing the mouse cochlear organoid system, we performed detailed metabolomic characterizations of the expanding and differentiating organoids. We found that hair cell differentiation is associated with increased mitochondrial electron transport chain (ETC) activity and reactive oxidative species generation. Transcriptome and metabolome analyses indicate reduced expression of oxidoreductases and tricyclic acid (TCA) cycle metabolites. The metabolic decoupling between ETC and TCA cycle limits the availability of the key metabolic cofactors, α-ketoglutarate and NAD+. Reduced expression of NAD+ in cochlear supporting cells by PGC1α deficiency further impairs hair cell reprogramming, while supplementation of α-ketoglutarate and NAD+ promotes hair cell reprogramming both in vitro and in vivo. Our findings reveal metabolic rewiring as a central cellular process during hair cell differentiation, and highlight the insufficiency of key metabolites as a metabolic barrier for efficient hair cell reprogramming.

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RNA-sequence facilitates analyze changes of P3 Plscr5 knockout mice

Project description:RNA-sequence facilitates analyze changes of P3 Plscr5 knockout mice

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RNA-sequence facilitates analyze changes of signaling pathways after drug treatment

Project description:Mammalian cochlear hair cells cannot regenerate after damage, which was a cause of hearing loss. Due to the small number of cochlear hair cells, we were unable to collect enough cells for research. Therefore, we have established a inner ear organoid model in this way, which greatly expands the number of supporting cells, Lgr5 and gradually mature hair cells. It can be used in high-throughput screening experiments. Using this model for high-throughput screening of FDA small molecule Drug, we found that Regorafenib can promote hair cell regeneration in vitro and get more mature regenerated hair cells. And we found that Regorfenib was though a new VEGF-TGFB axis to regulate hair cell regeneration.

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The H3K27 demethylase Utx facilitates somatic and germ cell epigenetic reprogramming to pluripotency

Project description:This SuperSeries is composed of the following subset Series: GSE35775: The H3K27 demethylase Utx facilitates somatic and germ cell epigenetic reprogramming to pluripotency [Affymetrix gene expression] GSE37821: The H3K27 demethylase Utx facilitates somatic and germ cell epigenetic reprogramming to pluripotency [ChIP-Seq] Refer to individual Series

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RNA-sequence facilitates analyze changes of P3 Plscr5 knockout mice

Project description:We report application of RNA-seq for transcriptomic analyses of cochlear tissues from wildtype and Plscr5 knockout mice to reveal gene expressions altered by Plscr5 knock out

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Netrin-1 facilitates somatic cell reprogramming by limiting Dcc pro-apoptotic activity.

Project description:The generation of induced pluripotent stem (iPS) cells holds great promise in regenerative medicine. However, the relative flaws in the understanding of the molecular mechanisms promoting or limiting reprogramming still hinder the efficient generation of high quality iPS cells. Whereas modulation of the initial Oct4, Sox2, Klf4 and c-Myc (OSKM) cocktail with new transcription factors has been extensively documented, comparatively little is known about soluble molecules promoting the process, even if such recombinant factors could be highly valuable for therapeutic applications. In this study we developed a large-scale identification method to uncover novel programmed cell death (PCD)-related mechanisms limiting somatic cell reprogramming to pluripotency (SCRP). We identified Netrin-1 and its dependence receptor Dcc (Deleted in Colorectal Carcinoma), previously described for their respective survival/death functions both in normal and oncogenic contexts, as novel key SCRP modulators. We show that the early phase of SCRP is accompanied with a strong Netrin-1 deficiency, due to the improper epigenetic regulation of the Ntn1 promoter by OSKM. Mechanistically, we demonstrate that such Netrin-1 imbalance induces apoptosis mediated by the dependence receptor Dcc in a p53-independent manner. Correction of the Netrin-1/Dcc equilibrium by gain-of-ligand and loss-of-receptor experiments constrains apoptosis and improves reprogramming. As a consequence, we propose a novel iPS derivation protocol including a sequential treatment with recombinant Netrin1 that greatly facilitates the generation of mouse and human iPS cells. RNA-sequencing of mouse embryonic fibroblasts (passage 2 and passage 4), mouse pre-iPS cells (passage 5 and passage 25), 1 clone of control iPS (passage 5 and passage 25) and 2 independent clones of "Netrin-1 derived" iPS cells (passage 5 and passage 25). For this analysis, mouse iPS cell lines were grown in KSR+LIF media.

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