scholarly journals ANXA1 directs Schwann cells proliferation and migration to accelerate nerve regeneration through the FPR2/AMPK pathway

2020 ◽  
Vol 34 (10) ◽  
pp. 13993-14005 ◽  
Author(s):  
Wenzheng Xia ◽  
Jin Zhu ◽  
Xueyi Wang ◽  
Yinda Tang ◽  
Ping Zhou ◽  
...  
Keyword(s):  
Nerve Regeneration ◽  
Schwann Cells ◽  
Ampk Pathway ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Leukemia inhibitory factor regulates Schwann cell proliferation and migration and affects peripheral nerve regeneration

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Qianqian Chen ◽  
Qianyan Liu ◽  
Yunsong Zhang ◽  
Shiying Li ◽  
Sheng Yi
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Peripheral Nerves ◽  
Leukemia Inhibitory Factor ◽  
Peripheral Nerve Regeneration ◽  
And Migration ◽  
Proliferation And Migration

AbstractLeukemia inhibitory factor (LIF) is a pleiotropic cytokine that stimulates neuronal development and survival. Our previous study has demonstrated that LIF mRNA is dysregulated in the peripheral nerve segments after nerve injury. Here, we show that LIF protein is abundantly expressed in Schwann cells after rat sciatic nerve injury. Functionally, suppressed or elevated LIF increases or decreases the proliferation rate and migration ability of Schwann cells, respectively. Morphological observations demonstrate that in vivo application of siRNA against LIF after peripheral nerve injury promotes Schwann cell migration and proliferation, axon elongation, and myelin formation. Electrophysiological and behavior assessments disclose that knockdown of LIF benefits the function recovery of injured peripheral nerves. Differentially expressed LIF affects the metabolism of Schwann cells and negatively regulates ERFE (Erythroferrone). Collectively, our observations reveal the essential roles for LIF in regulating the proliferation and migration of Schwann cells and the regeneration of injured peripheral nerves, discover ERFE as a downstream effector of LIF, and extend our understanding of the molecular mechanisms underlying peripheral nerve regeneration.

In Vitro Evaluation of the Growth and Migration of Schwann Cells on Electrospun Silk Fibroin Nanofibers

2011 ◽  
Vol 175-176 ◽  
pp. 220-223 ◽  
Author(s):  
Ai Jun Hu ◽  
Bao Qi Zuo ◽  
Feng Zhang ◽  
Qing Lan ◽  
Huan Xiang Zhang
Keyword(s):  
Tissue Engineering ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Schwann Cells ◽  
Silk Fibroin ◽  
Nerve Tissue ◽  
Nerve Tissue Engineering ◽  
And Migration ◽  
Silk Fibroin Nanofibers

Schwann cells (SCs) are primary structural and functional cells in peripheral nervous system and play a crucial role in peripheral nerve regeneration. Current challenge in peripheral nerve tissue engineering is to produce an implantable scaffold capable of bridging long nerve gaps and assist Scs in directing the growth of regenerating axons in nerve injury recovery. Electrospun silk fibroin nanofibers, fabricated for the cell culture in vitro, can provide such experiment support. Silk fibroin scaffolds (SFS) were fabricated with formic acid (FA), and the average fiber diameter was 305 ± 24 nm. The data from microscopic, immunohistochemical and scanning electron micrograph confirmed that the scaffold was beneficial to the adherence, proliferation and migration of SCs without exerting any significant cytotoxic effects on their phenotype. Thus, providing an experimental foundation accelerated the formation of bands of Bünger to enhance nerve regeneration. 305 nm SFS could be a candidate material for nerve tissue engineering.

scholarly journals DHI increases the proliferation and migration of Schwann cells through PI3K/AKT pathway and the expression of CXCL12 and GDNF to promote facial nerve function repair

2021 ◽  
Author(s):  
Dekun Gao ◽  
Lianhua Sun ◽  
Xiayu Sun ◽  
Jun Yang ◽  
Jingchun He
Keyword(s):  
Facial Nerve ◽  
Western Blot ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Akt Pathway ◽  
Nerve Function ◽  
Facial Nerve Function ◽  
Facial Nerve Injury ◽  
And Migration ◽  
Proliferation And Migration

Abstract BackgroundDanhong injection (DHI) is a commonly used drug in the treatment of cardiovascular and cerebrovascular diseases, and its neuroprotective research has been fully confirmed. Schwann cells, as myelin forming cells of peripheral nerve, play an important role in the process of injury and repair. The purpose of this study was to explore the effect of DHI on Schwann cells and its role in facial nerve injury.MethodsRSC 96 Schwann cells were treated with different concentrations (0 –2%) of DHI for different time intervals (12 and 36 h). Effect of DHI on cell viability and migration were determined by CCK8 and Transwell assays. The levels of PI3K-Akt signaling related proteins were measured by western blotting analysis, and the effects of DHI on GDNF and CXCL12 using Western Blot, RT-qPCR, and ELISA assays at the cellular and animal levels, respectively. Then LY294002, an inhibitor of PI3K, was used to study the effect of DHI on cell migration and secretion of CXCL12 and GDNF in RSC96 cells by Transwell, Western Blot, RT-qPCR, and ELISA assays. Finally, facial nerve scoring and S-100 immunofluorescence staining were used to study the therapeutic effects of DHI on facial nerve injury.ResultsOur study found that DHI can promote the proliferation and migration of RSC96 cells, and this effect is related to the activation of PI3K/AKT pathway. LY294002 inhibits the proliferation and migration of RSC96 cells. Besides, DHI can also promote the expression of CXCL12 and GDNF at gene and protein levels, and CXCL12 is, while GDNF is not, PI3K/AKT pathway-dependent. Animal experiments confirmed that DHI could promote CXCL12 and GDNF expression, and promote facial nerve function recovery and myelin regeneration. Conclusion Our in vitro and in vivo experiments demonstrated that DHI could promote proliferation and migration of Schwann cells through the PI3K/AKT pathway, and increase the expression of CXCL12 and GDNF to promote facial nerve function repair.

Sign in / Sign up

Export Citation Format

Share Document