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CircCRIM1/microRNA‐141‐3p/thioredoxin‐binding protein axis mediates neuronal apoptosis after cerebral ischemia‐reperfusion
Numerous studies have indicated enrichment of circular RNA (circRNA) in the brain takes on a momentous role in cerebral ischemia‐reperfusion (CIR) injury. A recent study discovered a novel circCRIM1, was highly expressed in the middle cerebral artery occlusion‐reperfusion (MCAO/R) model. Nevertheless, its specific biological function remained unknown. The study was to explore circCRIM1 in CIR‐induced neuronal apoptosis. As measured, circCRIM1 and TXNIP were up‐regulated, while miR‐141‐3p was down‐regulated in MCAO/R mouse model and OGD/R SH‐SY5Y cells. Depleting circCRIM1 reduced the number of apoptotic neurons in MCAO/R rats, increased the number of Nissl bodies, prevented reactive oxygen species production and oxidative stress imbalance in brain tissues, repressed cleaved caspase‐3, Bax, and Cyto C protein levels and increased Bcl‐2 levels. Overexpression of circCRIM1 further repressed neuronal activity and accelerated apoptosis in OGD/R model, disrupted redox balance. Depleting circCRIM1 had the opposite effect in OGD/R model. Knocking down miR‐141‐3p or TXNIP weakened the effects of knocking down circCRIM1 or overexpressing circCRIM1, separately. Mechanistically, circCRIM1 exerted an active role in CIR injury via miR‐141‐3p to mediate TXNIP. All in all, the circCRIM1/miR‐141‐3p/TXNIP axis might be a latent therapeutic target for CIR injury.
CircCRIM1/microRNA‐141‐3p/thioredoxin‐binding protein axis mediates neuronal apoptosis after cerebral ischemia‐reperfusion
Numerous studies have indicated enrichment of circular RNA (circRNA) in the brain takes on a momentous role in cerebral ischemia‐reperfusion (CIR) injury. A recent study discovered a novel circCRIM1, was highly expressed in the middle cerebral artery occlusion‐reperfusion (MCAO/R) model. Nevertheless, its specific biological function remained unknown. The study was to explore circCRIM1 in CIR‐induced neuronal apoptosis. As measured, circCRIM1 and TXNIP were up‐regulated, while miR‐141‐3p was down‐regulated in MCAO/R mouse model and OGD/R SH‐SY5Y cells. Depleting circCRIM1 reduced the number of apoptotic neurons in MCAO/R rats, increased the number of Nissl bodies, prevented reactive oxygen species production and oxidative stress imbalance in brain tissues, repressed cleaved caspase‐3, Bax, and Cyto C protein levels and increased Bcl‐2 levels. Overexpression of circCRIM1 further repressed neuronal activity and accelerated apoptosis in OGD/R model, disrupted redox balance. Depleting circCRIM1 had the opposite effect in OGD/R model. Knocking down miR‐141‐3p or TXNIP weakened the effects of knocking down circCRIM1 or overexpressing circCRIM1, separately. Mechanistically, circCRIM1 exerted an active role in CIR injury via miR‐141‐3p to mediate TXNIP. All in all, the circCRIM1/miR‐141‐3p/TXNIP axis might be a latent therapeutic target for CIR injury.
CircCRIM1/microRNA‐141‐3p/thioredoxin‐binding protein axis mediates neuronal apoptosis after cerebral ischemia‐reperfusion
Hu, Teng (author) / Li, Di (author) / Fan, TiePing (author) / Zhao, XuSheng (author) / Chen, ZhongJun (author)
Environmental Toxicology ; 38 ; 2845-2856
2023-12-01
12 pages
Article (Journal)
Electronic Resource
English
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