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RNAseq of mouse arthritic ankles with over-expression of miR-17-5p

ABSTRACT: RNAseq of mouse arthritic ankles with over-expression of miR-17-5p

PROVIDER: PRJNA578941 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10331007_1.fastq.gz	Fastqsanger.gz
	SRR10331007_2.fastq.gz	Fastqsanger.gz
	SRR10331008_1.fastq.gz	Fastqsanger.gz
	SRR10331008_2.fastq.gz	Fastqsanger.gz
	SRR10331009_1.fastq.gz	Fastqsanger.gz

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RNAseq of mouse arthritic ankles with over-expression of miR-17-5p

Project description:DBA1 mice with collagen-induced arthritis were injected intra-articularly with miR-17-5p mimic lipoplex. At the peak of inflammation (day 7), ankles were processed for bulk RNAseq using Illumina NextSeq 500.

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PETACC-8 miR-31-3p and miR-31-5p Ancillary Study

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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

Project description: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.

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Microarray of K562 cell line after overexpression of miR-15a-5p or miR-21-5p.

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Label free proteomic analysis of CAL62/miR-331-5p cells

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Gene expression changes induced by over-expression of miR-181b-5p in db/db mouse

Project description:The microRNAs (miRNAs) that can influence diabetic kidney disease (DKD) have not been fully characterized. The aim of this study was to identify the miRNAs that affect DKD and could be used as specific biomarkers or therapeutic agents. First, kidneys from two DKD mouse models were screened for differences in miRNA expression from control mice. We found that miRNA-125b-5p and miRNA-181-5p were specifically differentially expressed in the kidneys of DKD mice. Next, we administered miRNA-181b-5p-mimic to DKD mice, which reduced the albuminuria and abnormal mesangial expansion. Pathway analysis revealed that overexpression of miRNA-181-5p significantly altered the expression of 51 genes in the kidneys of DKD mice. Furthermore, the serum level of miRNA-125b-5p was significantly higher and that of miRNA-181-5p was lower in patients with DKD than in patients with other kidney diseases. These results suggest that miRNA-125b-5p and miRNA-181b-5p may represent novel diagnostic biomarkers and that miRNA-181b-5p may represent a therapeutic target for DKD.

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