LncRNA ZNF667-AS1 inhibits inflammatory response and promotes recovery of spinal cord injury via suppressing JAK-STAT pathway.

Abstract:

OBJECTIVE:The aim of this study was to explore the role of lncRNA ZNF667-AS1 in the recovery of spinal cord injury (SCI), and to investigate its underlying mechanism. MATERIALS AND METHODS:Mice were randomly assigned to the SCI group, the sham group and the lncRNA ZNF667-AS1 group, with 10 mice in each group. With Infinite Horizon device at a dose of 80 Kdyn, mice in the SCI group and the lncRNA ZNF667-AS1 group experienced SCI by an acute hit on the C5 spinous process. Before animal procedures, mice in the lncRNA ZNF667-AS1 group were additionally injected with overexpression lentivirus of lncRNA ZNF667-AS1. On the contrary, mice in the sham group only received laminectomy. After successful construction of the SCI model in mice, grip strength was accessed. LncRNA ZNF667-AS1 expression in spinal cord tissues before and after SCI was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), respectively. Meanwhile, the protein expression levels of relative genes in Janus Kinase-signal transducer and activator of transcription (JAK-STAT) pathway were detected by Western blot. RESULTS:Grip strength of forelimb in the SCI group recovered significantly slower than that of the sham group. With the prolongation of SCI, the expression of lncRNA ZNF667-AS1 was gradually decreased. However, the expression levels of JAK2, STAT3 and iNOS were upregulated in a time-dependent manner. In addition, mice in the lncRNA ZNF667-AS1 group presented remarkable grip strength recovery of forelimb after SCI. CONCLUSIONS:LncRNA ZNF667-AS expression is gradually downregulated after SCI. Meanwhile, it inhibits the inflammatory response and promotes SCI recovery via suppressing the JAK-STAT pathway.

authors

Li JW,Kuang Y,Chen L,Wang JF

doi

10.26355/eurrev_201811_16375

subject

Has Abstract

pub_date

2018-11-01 00:00:00

pages

7614-7620

issue

22

eissn

1128-3602

issn

2284-0729

journal_volume

22

pub_type

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