Fas Ligand Gene (Faslg) Plays an Important Role in Nerve Degeneration and Regeneration After Rat Sciatic Nerve Injury.

Yuting Li,Dengbing Yao,Shusen Cui,Nannan Gao,Huiwei Huang,Min Cai,Huanhuan Zhang,Yuhua Sun

doi:10.3389/fnmol.2018.00210

Abstract

Wallerian degeneration (WD) is associated with changes in the expression levels of a large number of genes. However, the effects of these up- or down-regulated genes are poorly understood. We have reported some key factors that are differentially regulated during WD in our previous research. Here, we explored the roles of Fas ligand gene (Faslg) in WD after rat sciatic nerve injury. The data showed that Faslg was up-regulated in injured nerves. Expression changed of Faslg in Schwann cells (SCs) resulted in alterations in the release of related factors. Silencing or overexpression of Faslg affected SC proliferation, migration, and apoptosis through β-catenin, nuclear factor-κB (NF-κB), and caspase-3 pathways in vivo and in vitro. Our data suggest that Faslg is a key regulatory gene that affects nerve repair and regeneration in peripheral nerve injury. This study sheds new light on the effects of Faslg on peripheral nerve degeneration and/or regeneration.

Highlights

Nerve injury is one of the most common clinical conditions and may be due to mechanical, chemical, congenital, or pathological causes (Noble et al, 1998; Kouyoumdjian, 2006; Valls-Sole et al, 2011; Zochodne, 2012)
The real-time quantitative polymerase chain reaction (qPCR) results indicated that Fas ligand gene (Faslg) expression was remarkably increased after injury
Faslg and S100B were colocalized in Schwann cell (SC), indicating that Faslg is expressed in SCss in the rat sciatic nerve

Summary

Introduction

Nerve injury is one of the most common clinical conditions and may be due to mechanical, chemical, congenital, or pathological causes (Noble et al, 1998; Kouyoumdjian, 2006; Valls-Sole et al, 2011; Zochodne, 2012). There are more than one million patients with peripheral nerve injury worldwide (Siemionow and Brzezicki, 2009). According to previous studies, injured nerves are capable of regeneration. The axon regeneration process is slow and proceeds at a rate of only 1–3 mm/day. Functional recovery is often poor (Sunderland, 1947; Frostick et al, 1998; Scholz et al, 2009).

Objectives

Methods

Results

Conclusion