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Review
. 2021 Dec 2:12:751021.
doi: 10.3389/fimmu.2021.751021. eCollection 2021.

Neuroinflammation and Scarring After Spinal Cord Injury: Therapeutic Roles of MSCs on Inflammation and Glial Scar

Affiliations
Review

Neuroinflammation and Scarring After Spinal Cord Injury: Therapeutic Roles of MSCs on Inflammation and Glial Scar

Qi-Ming Pang et al. Front Immunol. .

Abstract

Transected axons are unable to regenerate after spinal cord injury (SCI). Glial scar is thought to be responsible for this failure. Regulating the formation of glial scar post-SCI may contribute to axonal regrow. Over the past few decades, studies have found that the interaction between immune cells at the damaged site results in a robust and persistent inflammatory response. Current therapy strategies focus primarily on the inhibition of subacute and chronic neuroinflammation after the acute inflammatory response was executed. Growing evidences have documented that mesenchymal stem cells (MSCs) engraftment can be served as a promising cell therapy for SCI. Numerous studies have shown that MSCs transplantation can inhibit the excessive glial scar formation as well as inflammatory response, thereby facilitating the anatomical and functional recovery. Here, we will review the effects of inflammatory response and glial scar formation in spinal cord injury and repair. The role of MSCs in regulating neuroinflammation and glial scar formation after SCI will be reviewed as well.

Keywords: T cells; astrocyte; glial scar; macrophage; mesenchymal stem cells; neuroinflammation; spinal cord injury.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Primary and secondary injuries together leading to axonal regeneration failure and neuronal necrosis and apoptosis, results in dysfunction below the damaged plane in SCI patients.
Figure 2
Figure 2
MSCs transplantation promotes functional and anatomical recovery in SCI patients by inhibiting excessive inflammatory response and glial scar formation. Notes: ↑, promotion; ↓, inhibition.
Figure 3
Figure 3
Cellular and extracellular components of glial scar after SCI. Resident astrocytes, microglia and NG2 glia become migratory, proliferate, activated and lead to the glial scar after injury. Meanwhile, fibroblasts and circulating immune cells infiltrate into the damaged tissue and then increase the deposition of extracellular matrix molecules including extracellular matrix and CSGP. Glial scar can isolate the damaged spinal cord tissue, but it also limits the axonal plasticity.

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