Abstract
In spinal cord injury (SCI) therapy, glial scarring formed by activated astrocytes is a primary problem that needs to be solved to enhance axonal regeneration. In this study, we developed and used a collagen scaffold for glial scar replacement to create an appropriate environment in an SCI rat model and determined whether neural plasticity can be manipulated using this approach. We used four experimental groups, as follows: SCI-collagen scaffold, SCI control, normal spinal cord-collagen scaffold, and normal control. The collagen scaffold showed excellent in vitro and in vivo biocompatibility. Immunofluorescence staining revealed increased expression of neurofilament and fibronectin and reduced expression of glial fibrillary acidic protein and anti-chondroitin sulfate in the collagen scaffold-treated SCI rats at 1 and 4 weeks post-implantation compared with that in untreated SCI control. This indicates that the collagen scaffold implantation promoted neuronal survival and axonal growth within the injured site and prevented glial scar formation by controlling astrocyte production for their normal functioning. Our study highlights the feasibility of using the collagen scaffold in SCI repair. The collagen scaffold was found to exert beneficial effects on neuronal activity and may help in manipulating synaptic plasticity, implying its great potential for clinical application in SCI.
Highlights
Spinal cord injury (SCI) is a devastating condition encountered by neurosurgeons [1]
We found that the expression of SC-56 was remarkably decreased at 4 weeks post-implantation, suggesting that the collagen scaffold limited glial scar formation
We investigated the expression of CS-56, a specific marker of chondroitin sulfate proteoglycan, in the collagen scaffold-treated spinal cord injury (SCI) group (Figure 8)
Summary
Spinal cord injury (SCI) is a devastating condition encountered by neurosurgeons [1]. The major failures of axonal regeneration after injury are attributed to scar formation, a long-lasting inflammatory response, increasing levels of proteoglycans, and demyelination [2,3,4]. Among these factors, glial scar formation is considered a primary cause of Polymers 2020, 12, 2245; doi:10.3390/polym12102245 www.mdpi.com/journal/polymers. The mechanical trauma further leads to injury progression by facilitating recruitment and infiltration of non-resident cells with complex downstream signaling cascade effects on neuronal function and regeneration of myelin sheath [7,11]. The glial scar represents a physical and molecular barrier to axonal development and has become an important topic for research on tissue regeneration in chronic SCI [10,12,13]
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