Xiao et al. 2022 (PRJNA898430)
General Details
Title | IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury (OPC RiboTAG) |
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Organism | |
Number of Samples | 16 |
Release Date | 2022/11/04 00:00 |
Sequencing Types | |
Protocol Details |
Study Links
GWIPS-viz | Trips-Viz |
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Repository Details
SRA | SRP406387 |
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ENA | SRP406387 |
GEO | |
BioProject | PRJNA898430 |
Publication
Title | |
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Authors | Xiao G,Kumar R,Komuro Y,Burguet J,Kakarla V,Azizkhanian I,Sheth SA,Williams CK,Zhang XR,Macknicki M,Brumm A,Kawaguchi R,Mai P,Kaneko N,Vinters HV,Carmichael ST,Havton LA,DeCarli C,Hinman JD |
Journal | Cell reports |
Publication Date | 2022 Dec 20 |
Abstract | 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. Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved. |
PMC | PMC10026849 |
PMID | 36543124 |
DOI |
Run Accession | Study Accession | Scientific Name | Cell Line | Library Type | Treatment | GWIPS-viz | Trips-Viz | Reads | BAM | BigWig (F) | BigWig (R) | ||
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SRR22197716 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197717 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197714 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197715 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197712 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197713 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197710 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197711 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197708 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197709 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197706 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197707 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197704 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197705 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197702 | PRJNA898430 | Mus musculus | |||||||||||
SRR22197703 | PRJNA898430 | Mus musculus | |||||||||||
Run Accession | Study Accession | Scientific Name | Cell Line | Library Type | Treatment | GWIPS-viz | Trips-Viz | Reads | BAM | BigWig (F) | BigWig (R) |
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