Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 496, Issue 4, Pages 1302-1307Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2018.02.004
Keywords
Traumatic spinal cord injury (SCI); Spinal cord compression; Fibrotic scar; Wnt/beta-catenin signaling; TOPgal; Transgenic mice
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Funding
- Californian Institute for Regenerative Medicine (C.I.R.M.)
- Shriners Hospitals for Children [86600]
- NIH [1R01DE021696, 1R01DE026737]
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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.
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