Literature DB >> 29738767

miR-411 suppresses acute spinal cord injury via downregulation of Fas ligand in rats.

Zong-Ming Gong1, Zhen-Yu Tang2, Xiao-Liang Sun1.   

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 PC12 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 (P < 0.05). Similarly, the expression of miR-411 and FasL was significantly lower and higher in OGD group than that in control group, respectively (P < 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 (P < 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 (P < 0.05).
CONCLUSION: miR-411 mimic suppressed PC12 cell apoptosis via FasL, and relieved ASCI in rats.
Copyright © 2018. Published by Elsevier Inc.

Entities:  

Keywords:  Acute spinal cord injury (ASCI); Basso; Beattie and Bresnahan (BBB) score; Cell apoptosis; Fas ligand (FasL); Rat; miR-411

Mesh:

Substances:

Year:  2018        PMID: 29738767     DOI: 10.1016/j.bbrc.2018.05.022

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


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