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

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

PROVIDER: PRJNA898429 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22197700_1.fastq.gz	Fastqsanger.gz
	SRR22197700_2.fastq.gz	Fastqsanger.gz
	SRR22197701_1.fastq.gz	Fastqsanger.gz
	SRR22197701_2.fastq.gz	Fastqsanger.gz
	SRR22197702_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 (OPC RiboTAG)

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

| PRJNA898430 | ENA

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:This SuperSeries is composed of the SubSeries listed below.

2022-11-11 | GSE217356 | GEO

Comparative analysis of gene expression profile of pre-defined niches within demyelinated white matter in rats

Project description:Microenviromental niche characterization by comparative transcriptome profiling. The hypothesis tested in the present study was that unique properties of the perivascular niche within remyelinating white matter would create microenvironment that favor the alternative differentiation of oligodendrocyte precursor cells.

2018-09-14 | GSE93645 | GEO

Transcriptomic analyses of astrocyte heterogeneity within white matter tracts

Project description:Astrocytes are broadly categorized as protoplasmic or fibrous, with the former localized to synaptically dense gray matter regions and the latter associated with axons in the white matter. Much of what we know about astrocyte form and function is derived from the study of protoplasmic astrocytes, whereas fibrous astrocytes remain relatively unexplored. We investigated the transcriptome of uninjured fibrous astrocytes in the mouse from three regions: unmyelinated optic nerve head (ONH), myelinated optic nerve proper (ONP), and corpus callosum (CC).

2022-11-29 | GSE211515 | GEO

CXCL5 secreted from macrophages during cold exposure mediates white adipose tissue browning

Project description:Adipose tissue affects metabolic-related diseases as it consists of various types of cells that are involved in fat metabolism and adipokine release. CXC ligand 5 (CXCL5) is a member of the CXC chemokine family and is highly expressed by macrophages in white adipose tissue (WAT). In this study, we generated and investigated the function of Cxcl5 in knockout (KO) mouse. Cxcl5 KO mouse was generated using CRISPR/Cas9. The KO male mice didn’t show significant phenotype difference in normal condition. However, proteomic analysis revealed that many proteins are enriched in the process of fatty acid beta-oxidation and mitochondrial localization in iWAT of Cxcl5 KO mice. Cxcl5 KO mouse showed rather decreased proteins and transcripts expression associated with thermogenesis including uncoupled protein 1 (UCP1), a well-known thermogenic gene, and increased expressions associated with inflammation. The increase of Ucp1 expression in cold conditions was significantly retarded in Cxcl5 KO mice. The expression of transcription factors involved in thermogenesis including peroxisome proliferator-activated receptor gamma coactivator 1-alpha (Pgc1α) was not properly increased in Cxcl5 KO under cold challenge and its mimic conditions. CXCL5 treatment increased the expression of transcription factors for Ucp1 and Ucp1 itself. Collectively, our data shows that Ucp1 expression is induced in adipocyte by CXCL5 secreted by β-Adrenergic stimulation in M1 macrophages. Our data indicates that CXCL5 has a crucial role in regulating energy metabolism, particularly in cold exposure. These results strongly suggest that targeting CXCL5 could be a therapeutic aim for people with a disorder of energy metabolism.

2022-07-14 | PXD027291 | JPOST Repository

White Matter transcriptome in chronic alcoholism

Project description:Chronic alcohol consumption can lead to alchohol-related brain damage (ARBD). Despite the well known acute effects of alcohol the mechanism responsible for chronic brain damage is largely unknown. Pathologically the major change is the loss of white matter while neuronal loss is mild and restricted to a few areas such as the prefrontal cortex. In order to improve our understanding of ARBD pathogenesis we used microarrays to explore the white matter transcriptome of alcoholics and controls. Our results suggest that hepatic encephalopathy, along with two confounders, gray matter contamination and low RNA quality, are major drivers of gene expression in ARBD. All three exceeded the effects of alcohol itself. In particular, low quality RNA samples were characterized by an upregulation of protein translation machinery while hepatic encephalopathy was associated with a downregulation of mitochondrial energy metabolism pathways. The findings in HE alcoholics are consistent with the metabolic acidosis seen in this condition. In contrast non-HE alcoholics had widespread but only subtle changes in gene expression in their white matter. The initial cohort was compromised of four alcoholics without hepatic encephalopathy (non-HE alcoholics), three alcoholics with HE (HE alcoholics) and three neurologically normal controls. For each indvidual frozen white matter was sampled in the superior frontal gyrus (prefrontal cortex) and the precentral gyrus (motor cortex). These two cortices experience either moderate (prefrontal cortex) or no neuronal loss (motor cortex) with alcohol-related brain damage. Each white matter sample was divided in two before RNA was extracted to give two 'biological' repeats and a total of 40 samples. Subsequently eight duplicates were removed due to their gray matter contamination or low RNA quality to leave a 32-sample cohort (23 alcoholic (including eight with HE ) and nine control samples.

2014-01-04 | E-GEOD-53808 | biostudies-arrayexpress

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