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IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury (OPC RiboTAG)

ABSTRACT: IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury (OPC RiboTAG)

PROVIDER: PRJNA898430 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22197702_1.fastq.gz	Fastqsanger.gz
	SRR22197702_2.fastq.gz	Fastqsanger.gz
	SRR22197703_1.fastq.gz	Fastqsanger.gz
	SRR22197703_2.fastq.gz	Fastqsanger.gz
	SRR22197704_1.fastq.gz	Fastqsanger.gz

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IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury (OPC RiboTAG)

Project description:Cerebral small vessel disease and brain white matter injury are worsened by cardiovascular risk factors including obesity. Molecular pathways in cerebral endothelial cells activated by chronic cerebrovascular risk factors alter cell-cell signaling, blocking endogenous and post-ischemic white matter repair. Using cell-specific translating ribosome affinity purification(RiboTag) in white matter endothelia and oligodendrocyte progenitor cells (OPCs), we identify a coordinated interleukin-chemokine signaling cascade within the oligovascular niche of subcortical white matter that is triggered by diet-induced obesity (DIO).DIO induces IL-17B signaling that acts on the cerebral endothelia through IL-17Rb to increase both circulating and local endothelial expression of CXCL5. In white matter endothelia, CXCL5 promotes the association of OPCs with the vasculature and triggers OPC gene expression programs regulating cell migration through chemokine signaling. Targeted blockade of IL-17B reduced vessel-associated OPCs by reducing endothelial CXCL5 expression. In multiple human cohorts, blood levels of CXCL5 function as a diagnostic and prognostic biomarker of vascular cognitive impairment.

2022-11-11 | GSE217354 | GEO

IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury (Tie2-Cre RiboTAG)

2022-11-11 | GSE217355 | GEO

IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury (Tie2-Cre RiboTAG)

Project description:IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury (Tie2-Cre RiboTAG)

| PRJNA898432 | ENA

IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury.

Project description:Cerebral small vessel disease and brain white matter injury are worsened by cardiovascular risk factors including obesity. Molecular pathways in cerebral endothelial cells activated by chronic cerebrovascular risk factors alter cell-cell signaling, blocking endogenous and post-ischemic white matter repair. Using cell-specific translating ribosome affinity purification (RiboTag) in white matter endothelia and oligodendrocyte progenitor cells (OPCs), we identify a coordinated interleukin-chemokine signaling cascade within the oligovascular niche of subcortical white matter that is triggered by diet-induced obesity (DIO). DIO induces interleukin-17B (IL-17B) signaling that acts on the cerebral endothelia through IL-17Rb to increase both circulating and local endothelial expression of CXCL5. In white matter endothelia, CXCL5 promotes the association of OPCs with the vasculature and triggers OPC gene expression programs regulating cell migration through chemokine signaling. Targeted blockade of IL-17B reduced vessel-associated OPCs by reducing endothelial CXCL5 expression. In multiple human cohorts, blood levels of CXCL5 function as a diagnostic and prognostic biomarker of vascular cognitive impairment.

| S-EPMC10026849 | biostudies-literature

IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury

Project description:IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury

| PRJNA898429 | ENA

IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury

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

2022-11-11 | GSE217356 | GEO

Expression profile of OPC senescence

Project description:To identify factors involved in OPC senescence, we compared gene expressions between OPC-CG4, OPC-FCS and OPC-Rev. We established OPC senescence model system, in which OPC become senescent in the presence of high concentration of FCS. This phenotypes were kept even when the medium was switched to their optimal serum-free medium.

2011-06-01 | E-GEOD-28093 | biostudies-arrayexpress

Expression profile of OPC senescence

Project description:To identify factors involved in OPC senescence, we compared gene expressions between OPC-CG4, OPC-FCS and OPC-Rev.

2011-06-01 | GSE28093 | GEO

Normal and Oropharyngeal-carcinoma derived monocyte responses to OPC-cell line conditioned media.

Project description:Tumor Associated Macrophages (TAMs) represent a critical immunological barrier to effective anti-tumor mechanisms of developing carcinomas of the oropharynx. Tumor infiltrating monocytes become activated and differentiate into TAMs which contribute to the immunological landscape of tumors as either containing or devoid of effector T-cells. We first compared transcriptional responses of normal and OPC derived monocytes from single individuals, at the single cell level, after exposure to media conditioned by SCC-25 and SCC-154 OPC cell lines. Since media conditioned by both SCC-154 and SCC-25 contain secreted IL1α, stimulation of these monocytes with recombinant IL1α was included as a control. We showed that to these conditioned media, CXCL1, CXCL5 and CCL2 transcripts reached higher levels in a greater proportion of OPC-patient monocytes compared to control monocytes. These early monocyte responses were validated in a cohort of isolated monocytes exposed to the same media. These findings represent that monocytes may be secreting TME influencing cytokines, prior to their own differentiation, which in turn recruit detrimental cell populations including T-regs, MDSCs and other monocytes.

2024-11-25 | GSE281098 | GEO

LPC 18:1 protein interaction (OPC)

Project description:Oligodendrocyte progenitor cells (OPC) were cultured in the presence of LPC 18:1-Cy5. Proteins interacting with LPC 18:1-Cy5 were UV crossed linked and cell lysates were separated via isoelectric focusing gel electrophoresis. Band was cut out from gel and processed for mass spectrometry. OPC lysates were also incubated with LPC 18:1-micelles and allowed to interact with OPC proteins. Samples were separated using sucrose gradient (Liposome floatation assay), top fraction was collected and processed for mass spectrometry.

2022-02-17 | PXD025175 | Pride

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