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CircRIMS promotes cerebral ischemia-reperfusion injury through increasing apoptosis and targeting the miR-96-5p/JAK/STAT1 axis.
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- Author(s): Li, Wei; Xie, Lin; Wang, Lisha; Lin, Faliang
- Source:
Brain Injury. 2023, Vol. 37 Issue 11, p1235-1244. 10p. - Source:
- Additional Information
- Subject Terms: CIRCULAR RNA; STAT proteins; IN vitro studies; BIOLOGICAL models; DISEASE progression; FLOW cytometry; ANIMAL experimentation; INFLAMMATION; APOPTOSIS; MICRORNA; GENE expression; JANUS kinases; CELLULAR signal transduction; CEREBRAL arteries; CELL survival; GENE expression profiling; LACTATE dehydrogenase; CEREBRAL ischemia; REPERFUSION injury; MICE
- Abstract: This study aims to explore the function of circRIMS in cerebral ischemia/reperfusion (CIR) and its regulatory mechanism. The expression of the circRIMS was examined in GEO chip data and validated by qRT-PCR analysis. A middle cerebral artery occlusion/repression (MCAO/R) model was developed using C57BL/6J mice. Starbase and circinteractome were employed to identify the target miRNA and mRNA. The result was confirmed by dual-luciferase reporter assay, and biotinylated RNA-pulldown assay. The cell viability and apoptosis were confirmed through CCK-8 and flow cytometry assay. This study revealed that circRIMS expression was upregulated in MCAO mice model and OGD/RX-simulated cell model. Knockdown circRIMS demonstrated the functional of circRIMS in increasing cell viability, reducing apoptosis, LDH activity and inflammatory factors secretion in OGD/RX-simulated CIR injury in vitro. Additionally, miR-96-5p was identified as a target of circRIMS, while the STAT1 gene is a downstream gene of miR-96-5p, and JAK was also considered to be a downstream gene of the JAK-STAT pathway. Furthermore, inhibition of miR-96-5p or overexpression of STAT1 promoted the progression of CIR injury by elevating apoptosis, reducing cell viability, and increasing the secretion of inflammatory cytokines. CircRIMS contributes to the progression of CIR injury via regulating miR-96-5p/JAK/STAT1 axis. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Brain Injury is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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