miR-411 suppresses acute spinal cord injury via downregulation of Fas ligand in rats.
Biochem Biophys Res Commun
; 501(2): 501-506, 2018 06 22.
Article
en En
| MEDLINE
| ID: mdl-29738767
ABSTRACT
OBJECTIVE:
To explore the role of miR-411/FasL in acute spinal cord injury (ASCI).METHODS:
The ASCI rat model was established, and expression of miR-411 and Fas ligand (FasL) was examined. Basso, Beattie and Bresnahan (BBB) score was used to evaluate the rats' neurological function. PC12 oxygen-glucose deprivation (OGD) model was also established. Gene manipulation (including miR-411 mimic or inhibitor) was used to modulate gene expression. Luciferase reporter assay was conducted to confirm the targeting relationship between miR-411 and FasL. Flow cytometry was applied in the measurement of PC12â¯cell apoptosis. Finally, the miR-411 mimic was injected into the vertebral canal of ASCI rats to determine the effects of miR-411 in vivo.RESULTS:
Compared with sham group, the expression of miR-411 and FasL was significantly decreased and increased in ASCI group, respectively (Pâ¯<â¯0.05). Similarly, the expression of miR-411 and FasL was significantly lower and higher in OGD group than that in control group, respectively (Pâ¯<â¯0.05). miR-411 directly controlled the FasL expression. miR-411 mimic can dramatically reduce the increased percentage of apoptosis cells caused by OGD when comparing to mimic control, which was greatly reversed by the overexpression of FasL (Pâ¯<â¯0.05). Further, the BBB score was significantly elevated in the miR-411 mimic group when comparing to mimic control group, with decreased FasL expression (Pâ¯<â¯0.05).CONCLUSION:
miR-411 mimic suppressed PC12â¯cell apoptosis via FasL, and relieved ASCI in rats.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Traumatismos de la Médula Espinal
/
Regulación hacia Abajo
/
MicroARNs
/
Proteína Ligando Fas
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
2018
Tipo del documento:
Article
País de afiliación:
China