Foxp3 attenuates cerebral ischemia/reperfusion injury through microRNA-150-5p-modified NCS1.
Exp Cell Res
; : 112942, 2021 Nov 22.
Article
em En
| MEDLINE
| ID: mdl-34822811
ABSTRACT
OBJECTIVE:
Cerebral ischemia/reperfusion injury (CI/RI) is a pathological process involving complicated molecular mechanisms. We investigated forkhead box P3 (Foxp3)-related mechanism in CI/RI with particular focus on microRNA (miR)-150-5p/nucleobase cation symporter-1 (NCS1) axis.METHODS:
A mouse model was constructed by middle cerebral artery occlusion (MCAO) method. Levels of Foxp3, miR-150-5p and NCS1 were assessed in brain tissues of MCAO mice. By determining the neurological behavior function, neurological deficits, brain tissue pathological characteristics, neuronal apoptosis, inflammatory factors, and oxidative stress-related factors, the functional role of Foxp3, miR-150-5p and NCS1 were evaluated in MCAO mice. The feedback loop was analyzed among Foxp3, miR-150-5p and NCS1.RESULTS:
The level of Foxp3 and NCS1 were reduced and that of miR-150-5p was augmented in MCAO mice. Foxp3 bound to miR-150-5p to target NCS1. Up-regulating Foxp3 or NCS1 or suppressing miR-150-5p improved neurological behavior function and neurological deficits, and reduced brain tissue pathological damage, neuronal apoptosis, inflammatory and oxidative stress reactions in MCAO mice. Silencing miR-150-5p or elevating NCS1 decreased Foxp3 silencing-mediated ischemic injury in MCAO mice.CONCLUSION:
Foxp3 is neuroprotective in CI/RI through binding to miR-150-5p to promote NCS1 expression.
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Base de dados:
MEDLINE
Tipo de estudo:
Prognostic_studies
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article