Transient activation of Wnt/β-catenin signaling reporter in fibrotic scar formation after compression spinal cord injury in adult mice

被引:16
作者
Yamagami, Takashi [1 ,2 ]
Pleasure, David E. [2 ]
Lam, Kit S. [1 ]
Zhou, Chengji J. [1 ,2 ]
机构
[1] Univ Calif Davis, Dept Biochem & Mol Med, Sch Med, Sacramento, CA 95817 USA
[2] UC Davis Sch Med, Inst Pediat Regenerat Med, Shriners Hosp Children Northern Calif, Sacramento, CA 95817 USA
关键词
Traumatic spinal cord injury (SCI); Spinal cord compression; Fibrotic scar; Wnt/beta-catenin signaling; TOPgal; Transgenic mice; CENTRAL-NERVOUS-SYSTEM; AXON REGENERATION; REACTIVE ASTROCYTES; GLIAL SCAR; CNS; REPAIR; DIFFERENTIATION; NEUROGENESIS; INHIBITION; GUIDANCE;
D O I
10.1016/j.bbrc.2018.02.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
After traumatic spinal cord injury (SCI), a scar may form with a fibrotic core (fibrotic scar) and surrounding reactive astrocytes (glial scar) at the lesion site. The scar tissue is considered a major obstacle preventing regeneration both as a physical barrier and as a source for secretion of inhibitors of axonal regeneration. Understanding the mechanism of scar formation and how to control it may lead to effective SCI therapies. Using a compression-SCI model on adult transgenic mice, we demonstrate that the canonical Wnt/beta-catenin signaling reporter TOPgal (TCF/Lefl-lacZ) positive cells appeared at the lesion site by 5 days, peaked on 7 days, and diminished by 14 days post injury. Using various representative cell lineage markers, we demonstrate that, these transiently TOPgal positive cells are a group of Fibronectin(+);GFAP(-) fibroblast-like cells in the core scar region. Some of them are proliferative. These results indicate that Wnt/beta-catenin signaling may play a key role in fibrotic scar formation after traumatic spinal cord injury. (C) 2018 Elsevier Inc. All rights reserved.
引用
收藏
页码:1302 / 1307
页数:6
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