Asset Details
Do you wish to reserve the book?
MicroRNA-29b-3p promotes endothelial cell inflammation via NTRK2/PI3K/NLRP3 pathway in Moyamoya disease
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
MicroRNA-29b-3p promotes endothelial cell inflammation via NTRK2/PI3K/NLRP3 pathway in Moyamoya disease
Do you wish to request the book?
MicroRNA-29b-3p promotes endothelial cell inflammation via NTRK2/PI3K/NLRP3 pathway in Moyamoya disease
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
MicroRNA-29b-3p promotes endothelial cell inflammation via NTRK2/PI3K/NLRP3 pathway in Moyamoya disease
2025
Overview
Moyamoya disease (MMD) is a rare chronic progressive vascular anomaly of the skull base whose molecular regulatory mechanisms remain poorly understood. We therefore aimed to analyze the molecular mechanisms involved in the development of MMD from the perspective of miRNA regulation of mRNA. Raw gene expression profiles (GSE178501, GSE157628 and GSE189993) were downloaded from the Gene Expression Omnibus database and used to identify differentially expressed genes and perform functional enrichment analysis. Differentially expressed miRNAs and their predicted target genes were validated by RT-qPCR. Oxygen glucose deprivation was applied to induce an inflammatory injury cell model in human brain microvascular endothelial cells (BMEC). 973 differentially expressed mRNAs and 3 differentially expressed miRNAs were identified in three sets of gene expression profiles. RT-qPCR confirmed that the
miR-29b-3p
was upregulated in leukocytes of MMD and that the expression of
NTRK2
was downregulated. Dual-luciferase reporter assay indicated that
NTRK2
was the direct target of
miR-29b-3p
. Overexpression of
NTRK2
improved the viability of BMEC and increased the protein levels of NTRK2 and pPI3K, while suppressed the expression of NLRP3, IL1β, and TNF-α.
miR-29b-3p
treatment partially abolished the protective effect of
NTRK2
and diminished the effect of NTRK2 on PI3K/NLRP3 pathway. In conclusion, this study provided a novel insight into the pathophysiological mechanisms of MMD and demonstrated that the
miR-29b-3p
/
NTRK2
/PI3K/NLRP3 axis plays a pivotal role in the progression of MMD.
Publisher
BioMed Central,BioMed Central Ltd,BMC
Subject
/ Endothelial Cells - metabolism
/ Endothelial Cells - pathology
/ Genes
/ Humans
/ Medicine
/ MicroRNA
/ Moyamoya
/ Moyamoya Disease - metabolism
/ Moyamoya Disease - pathology
/ NLR Family, Pyrin Domain-Containing 3 Protein - genetics
/ NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
/ NLRP3
/ NTRK2
/ Oncology
/ Phosphatidylinositol 3-Kinases - genetics
/ Phosphatidylinositol 3-Kinases - metabolism
/ Surgery
