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Series GSE266940 Query DataSets for GSE266940
Status Public on May 12, 2024
Title Extracellular vesicles from early- and late-passage endothelial cells differentially regulate cerebrovascular and brain aging in mice via changes in a miR-17-5p-dependent pathway
Organism Mus musculus
Experiment type Non-coding RNA profiling by high throughput sequencing
Summary Vascular aging, which is characterized by brain endothelial cell (EC) senescence and dysfunction, is known to contribute to various age-related cerebrovascular and neurodegenerative diseases. However, the underlying mechanisms remain unclear. EC-derived microvesicles (EMVs) and exosomes (EEXs) retain the characteristics of parent cells and transfer their contents to modulate the functions of recipient cells, showing potential for evaluation or regulation of vascular aging. Here, as indicated by analyses of senescence-associated beta-galactosidase (SA-β-gal) staining, cerebral blood flow, blood–brain barrier function, aging-related markers and cognitive ability, we found that young primary EC (passage 2-4) released EMVs alleviated mouse cerebrovascular and brain aging more effectively than EEXs. Aged EC (passage 15-16) released EMVs were more effective than their released EEXs at exacerbating mouse cerebrovascular and brain aging. We further revealed that these EMVs regulated cerebrovascular and brain aging by transferring miR-17-5p and modulated EC senescence and function via the miR-17-5p/PI3K/Akt pathway. Clinically, the levels of plasma EMVs and their associated miR-17-5p (EMV-miR-17-5p) were significantly increased or decreased in elderly individuals and were closely correlated with reactive oxygen species (ROS) and vascular aging. Receiver operating characteristic (ROC) analysis revealed that the area under the curve (AUC) was 0.724 for EMVs, 0.77 for EMV-miR-17-5p and 0.815 for their combination for distinguishing vascular aging. Our results identified novel roles for EMVs and showed that these vesicles more effectively modulated vascular and brain aging than did EEXs by regulating EC functions through the miR-17-5p/PI3K/Akt pathway; thus, EMVs and EMV-miR-17-5p are promising biomarkers and therapeutic targets for vascular aging.
 
Overall design To investigate the mechanism of different effects of EMV from young and old endothelial cells (y.EMVs and o.EMVs). MiRNA sequencing was applied to identify the functional miRNAs in EMVs. Comparative gene expression profiling analysis of RNA-seq data for y.EMVs (derived from passage 2-5 primary endothelial cells) and o.EMVs (derived from passage 15-16 primary endothelial cells))
 
Contributor(s) Zhang H
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Submission date May 07, 2024
Last update date May 12, 2024
Contact name Huiting Zhang
E-mail(s) barbara3367723@126.com
Phone +86 2387427
Organization name The Affiliated Hospital of Guangdong Medical University
Department Neurological department
Street address No. 57 People's Road South, Xiashan District
City Zhanjiang
State/province Guangdong
ZIP/Postal code 524000
Country China
 
Platforms (1)
GPL21273 HiSeq X Ten (Mus musculus)
Samples (4)
GSM8257225 y.EMVs derived from passage 2-3 primary brain microvascular ECs
GSM8257226 y.EMVs derived from passage 3-4 primary brain microvascular ECs
GSM8257227 o.EMVs derived from passage 15 primary brain microvascular ECs
Relations
BioProject PRJNA1108752

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE266940_miRNA_reads_count.txt.gz 4.8 Kb (ftp)(http) TXT
SRA Run SelectorHelp
Raw data are available in SRA

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