Effects of microRNA-338 Transfection into Sciatic Nerve on Rats with Experimental Autoimmune Neuritis

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Effects of microRNA-338 Transfection into Sciatic Nerve on Rats with Experimental Autoimmune Neuritis Xiaojing Yuan 1 & Yujun Wei 2 & Tianrang Ao 2 & Kai Gong 2 & Qiangsan Sun 3 & Zuncheng Zheng 1 & Haruo Hagiwara 4 & Qiang Ao 5,6 Received: 20 May 2020 / Accepted: 17 August 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020

Abstract Nerve demyelination or axonal lesions are characteristic of experimental autoimmune neuritis (EAN). Previous studies have demonstrated that microRNA-338 can regulate the differentiation and maturation of oligodendrocytes and Schwann cells and promote injured peripheral nerves in rats. In this study, we used microRNA-338 coded lentivirus vector (miR-338-LV) in a Lewis rat EAN model, in with the conjunction P0 peptide 180–199 which was injected into the footpads of animals to induce immunization. The clinical scores of miR-338-LV and intravenous immunoglobulin (IVIg) (positive drug) groups were significantly superior to those of untreated group at disease peak and disease plateau (p < 0.05). The nerve conduction velocity and the compound nerve action potential amplitude of miR-338-LV and IVIg groups increased significantly compared to those of the untreated group at disease peak (p < 0.01). At disease peak, myelin swelling, cavity formation, and lamellae separation showed improvement in miR-338-LV and IVIg groups compared to untreated group. S100 and NF200 expression in miR-338-LV and IVIg groups increased compared to that in untreated group. Iba1 and S100 co-expression in Schwann cells in miR-338-LV and IVIg groups decreased compared to that in untreated group, which was indicative of the reduced conversion of Schwann cells into inflammatory cells. Overall, miR-338-LV in sciatic nerves might improve neuromuscular function in EAN by inhibiting the conversion of Schwann cells into inflammatory cells. Keywords microRNA-338 . Experimental autoimmune neuritis . Schwann cell . Sciatic nerve . Myelin ultrastructure . Intravenous immunoglobulin (IVIg)

Introduction

* Zuncheng Zheng [email protected] * Qiang Ao [email protected] 1

Department of Rehabilitation, Taian City Central Hospital, Taian 271000, Shandong, China

2

College of life science, Tsinghua University, Beijing 100084, China

3

Department of Rehabilitation, The Second Hospital, Jinan 250033, Shandong, China

4

Department of Anatomy and Cell Biology, Teikyo University School of Medicine, Tokyo, Japan

5

Institute of Regulatory Science for Medical Device, Sichuan University, Chengdu, China

6

National Engineering Research Center for Biomaterials, Sichuan University, Chengdu 610064, China

Guillain-Barré Syndrome (GBS) is a disease with a variety of clinical types (Peric et al. 2014; Siu et al. 2016; Gao et al. 2018), and the main pathological features are peripheral nerve demyelination or axonal lesions(Peric et al. 2014). This disease is characterized by a directed autoimmune reaction against specific components of peripheral nerves(Wang et al. 2014; Talukder et al. 2011; Huang et al. 2018