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Role of chondroitin sulfate proteoglycan signaling in regulating neuroinflammation following spinal cord injury 被引量:4

Role of chondroitin sulfate proteoglycan signaling in regulating neuroinflammation following spinal cord injury
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摘要 Spinal cord injury (SCI) elicits a robust inflammatory response that is a hallmark of the secondary injury mechanisms. Neuroinflammation is orchestrated initially by the response of resident astrocytes and microglia to injury, which subsequently facilitates the recruitment of peripheral immune cells into the SCI lesion (Orr and Gensel, 2018). This inflammatory response contributes to cell death and tissue degeneration through the production of pro-inflammatory cytokines and chemokines, free radicals and proteolytic enzymes. However, neuroinflammatory cells also play beneficial regulatory role in repair mechanisms after SCI by adopting a reparative and wound healing phenotype (Orr and Gensel, 2018; Tran et al., 2018). Hence, understanding the underlying mechanisms by which immune cells are reg- ulated within the microenvironment of injury would aid in harnessing the reparative potential of inflammation following SCI. Spinal cord injury (SCI) elicits a robust inflammatory response that is a hallmark of the secondary injury mechanisms. Neuroinflammation is orchestrated initially by the response of resident astrocytes and microglia to injury, which subsequently facilitates the recruitment of peripheral immune cells into the SCI lesion (Orr and Gensel, 2018). This inflammatory response contributes to cell death and tissue degeneration through the production of pro-inflammatory cytokines and chemokines, free radicals and proteolytic enzymes. However, neuroinflammatory cells also play beneficial regulatory role in repair mechanisms after SCI by adopting a reparative and wound healing phenotype (Orr and Gensel, 2018; Tran et al., 2018). Hence, understanding the underlying mechanisms by which immune cells are reg- ulated within the microenvironment of injury would aid in harnessing the reparative potential of inflammation following SCI.
出处 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第12期2080-2082,共3页 中国神经再生研究(英文版)
基金 supported by the Craig H.Neilsen Foundation awarded to SKA supported by a joint studentship from Will-to-Win/Manitoba Paraplegic Foundation the Children’s Hospital Research Institute of Manitoba
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