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Transcriptional changes in human haematopoietic stem and progenitor cells（HSPCs） from umbilical cord blood in response to the corticotropin releasing hormone（CRH）

ABSTRACT: Transcriptional changes in human haematopoietic stem and progenitor cells（HSPCs） from umbilical cord blood in response to the corticotropin releasing hormone（CRH）

PROVIDER: PRJNA1002307 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25528127_1.fastq.gz	Fastqsanger.gz
	SRR25528127_2.fastq.gz	Fastqsanger.gz
	SRR25528128_1.fastq.gz	Fastqsanger.gz
	SRR25528128_2.fastq.gz	Fastqsanger.gz
	SRR25528129_1.fastq.gz	Fastqsanger.gz

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Transcriptional changes in human haematopoietic stem and progenitor cells（HSPCs） from umbilical cord blood in response to the corticotropin releasing hormone（CRH）

Project description:Corticotrophin-releasing hormone (CRH) is a key regulator involved in the stress pathway, yet its functions in the direct regulation of human stem/ progenitor cells (HSPCs) are poorly understood. Here we report that human CD34+ HSPCs constitutively expressed CRH receptor1. Treatment with CRH increased the motility and deformability of human HSPCs. Intravital two-photon imaging of bone tissues showed that CRH stimulated migration and bone marrow homing of HSPCs in vivo. Pretreatment of human HSPCs promoted homing and long-term engraftment when transplanted into primary and secondary NSG mice. Mechanistically, CRH modulates cell mechanics by extracellular matrix (ECM) remodeling, correlating with increased expression of the ECM protein THBS2 and activities of the Rho family small GTPases. Collectively, these findings show that CRH, a neurotransmitter, regulates biomechanics, which is correlated with its new functions in HSPSs migration, homing and engraftment, designating CRH as a promising drug candidate to facilitate clinical HSC transplantation.

2023-09-01 | GSE240116 | GEO

Primary Trophoblasts treated with Corticotropin Releasing Hormone (CRH)

Project description:Primary trophoblast cells were treated with corticotropin releasing hormone (CRH) and then subjected to RNA extraction and sequencing.

2025-03-13 | GSE279747 | GEO

Primary Trophoblasts treated with Corticotropin Releasing Hormone (CRH)

Project description:Primary Trophoblasts treated with Corticotropin Releasing Hormone (CRH)

| PRJNA1174194 | ENA

Transcriptional effect of CRH on MCF7 estrogen receptor signalling

2013-07-02 | GSE47958 | GEO

Transcriptional effect of CRH on MCF7 estrogen receptor signalling

Project description:MCF7 cells were stimulated with vehicle or 100nM corticotropin releasing hormone (CRH) for 24h. The effect of CRH on the expression of genes relevant to estrogen signalling was investigated by using the Human Estrogen Receptor Signaling RTM-BM-2 ProfilerM-bM-^DM-" PCR Array (SABioscience Corp). qPCR gene expression profiling. MCF7 cells were treated separately in triplicate. Equal amount total RNA was processed further for gene expression analysis.

2013-07-02 | E-GEOD-47958 | biostudies-arrayexpress

Placenta and uterus transcriptomes from transgenic mice expressing human corticotropin-releasing hormone in placenta

Project description:Purpose: Parturition is delayed by approximately 12 hours in transgenic mice expressing human corticotropin-releasing hormone (CRH) in placenta. The goal of the study was to identify the pathways in reproductive tissues (uterus and placenta) altered by placental expression of human CRH. Methods: Human BAC RP11-366K18 (CHORI) containing human CRH and cis-regulatory region was inserted into the mouse genome by microinjection and random integration to create the BAC1 line. The CRISPR/Cas9 system was used to delete a CRH regulatory element from the BAC1 line to create the CR1 line, eliminating expression of CRH in placenta. Total expression of uterus and placenta by RNA-seq at embryonic day 18.5 were compared between BAC1, CR1, and nontransgenic mice. Results: Genes known to be associated with luteolysis and initiation of parturition (Cav1, Gja1, Oxtr, Ptgs1, Ptgs2) were not differentially expressed in uterus of this model. Conclusions: CRH-mediated delay of parturition is likely independent of luteolysis.

2018-08-09 | GSE118283 | GEO

Cell-Specific Transcriptomic Analysis of CRH+ cells Identifies Unique Cellular Responses to Chronic Stress

Project description:Rationale: A previous transcriptome meta-analysis revealed significantly lower levels of corticotropin-releasing hormone (CRH) mRNA in corticolimbic brain regions in major depressive disorder (MDD) subjects. Rodent studies show that cortical CRH is mostly expressed in GABAergic neurons; however, the characteristic features of CRH+ cells in human brain cortex and their association with MDD are largely unknown. Methods: Subgenual anterior cingulate cortex (sgACC) of human subjects without brain disorders were labeled using fluorescent in situ hybridization (FISH) for CRH and markers of excitatory (SLC17A7), inhibitory (GAD1) neurons, as well as markers of other interneuron subpopulations (PVALB, SST, VIP). MDD-associated changes in CRH+ cell density and cellular CRH expression (n=6/group) were analyzed. RNA-sequencing was performed on sgACC CRH+ neurons from comparison and MDD subjects (n=6/group), and analyzed for group differences. Results: About 80% of CRH+ cells were GABAergic and 17.5% were glutamatergic. CRH+ GABAergic neurons co-expressed VIP (52%), SST (7%), or PVALB (7%). MDD subjects displayed lower CRH mRNA levels in GABAergic neurons relative to comparison subjects without changes in cell density. CRH+ neurons show transcriptomic profile suggesting lower excitability and less GABA release and reuptake. Further analyses suggested that these molecular changes are not mediated by altered glucocorticoid feedback and potentially occur downstream for a common modulator of neurotrophic function. Summary: CRH+ cells in human sgACC are a heterogeneous population of GABAergic neurons, although largely co-expressing VIP. MDD is associated with reduced markers of inhibitory function of CRH+ neurons.

2022-02-22 | GSE193417 | GEO

Single-cell transcriptome analysis of secretagogin mRNA expressing cells from the mouse hypothalamic paraventricular nucleus

Project description:The molecular mechanism regulating phasic corticotropin-releasing hormone (CRH) release from parvocellular neurons (PVN) remains poorly understood. Here, we find a cohort of parvocellular cells interspersed with magnocellular PVN neurons expressing secretagogin. Single-cell transcriptome analysis combined with protein interactome profiling identifies secretagogin neurons as a distinct CRH-releasing neuron population reliant on secretagoginM-bM-^@M-^Ys Ca2+ sensor properties and protein interactions with the vesicular traffic and exocytosis release machineries to liberate this key hypothalamic releasing hormone. single cells from the PVN region juvenile (21-28 days) mice were dissected and subject to whole transcriptome analysis

2014-11-20 | E-GEOD-63093 | biostudies-arrayexpress

Single-cell transcriptome analysis of secretagogin mRNA expressing cells from the mouse hypothalamic paraventricular nucleus

Project description:The molecular mechanism regulating phasic corticotropin-releasing hormone (CRH) release from parvocellular neurons (PVN) remains poorly understood. Here, we find a cohort of parvocellular cells interspersed with magnocellular PVN neurons expressing secretagogin. Single-cell transcriptome analysis combined with protein interactome profiling identifies secretagogin neurons as a distinct CRH-releasing neuron population reliant on secretagogin’s Ca2+ sensor properties and protein interactions with the vesicular traffic and exocytosis release machineries to liberate this key hypothalamic releasing hormone.

2014-11-20 | GSE63093 | GEO

Connect-seq to superimpose molecular on anatomical neural circuit maps

Project description:We report RNA sequencing of single virus-infected neurons upstream of neurons producing corticotropin-releasing hormone (CRH). Analyses of PRV-infected transcriptomes reveal neurons upstream of CRH neurons express diverse and a large variety of signaling molecules. The molecular identities of upstream neurons can be used to superimpose a molecular on neuroanatomical circuit maps.

2019-11-06 | GSE139923 | GEO

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