Journal
MOLECULAR NEUROBIOLOGY
Volume 53, Issue 9, Pages 5912-5927Publisher
HUMANA PRESS INC
DOI: 10.1007/s12035-015-9486-6
Keywords
Astrogliosis; C/EBPd; MMP-3; RhoA; Astrocyte migration
Categories
Funding
- Ministry of Science and Technology, Taiwan [103-2321-B-006-031, 103-2320-B-006-034-MY3, 101-2320-B-006-008-MY3]
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After spinal cord injury, inflammatory reaction induces the aggregation of astrocytes to form a glial scar that eventually blocks axonal regeneration. Transcription factor CCAAT/enhancer-binding protein delta (C/EBP delta) is a regulatory protein of genes responsive to inflammatory factors, but its role in glial scar formation after spinal cord injury remains unknown. By using a model of moderate spinal cord contusion injury at the mid-thoracic level, we found that C/EBP delta was expressed mostly in the reactive astrocytes bordering the lesion in wild-type mice from 7 days after the injury. C/EBP delta-deficient mice showed reduced glial scar formation, more residual white matter, and better motor function recovery compared with wild-type mice 28 days after the injury. Upon interleukin (IL)-1 beta stimulation in vitro, the increased expression of C/EBP delta in reactive astrocytes inhibited RhoA expression and, subsequently, the ability of astrocyte migration. However, these reactive astrocytes also produced an increased amount of matrix metalloproteinase-3, which promoted the migration of non-IL-1 beta-treated, inactive astrocytes. Although the involvement of other non-astroglial C/EBP delta cannot be entirely excluded, our studies suggest that astrocytic C/EBP delta is integral to the inflammatory cascades leading to glial scar formation after spinal cord injury.
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