The Glial Cells Respond to Spinal Cord Injury

Wang, Ruideng; Zhou, Rubing; Chen, Zhengyang; Gao, Shan; Zhou, Fang

doi:10.3389/fneur.2022.844497

Cited by 15 publications

(12 citation statements)

References 168 publications

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“… 110 While glia are important in the response to SCI, there is a delicate balance between pro- and anti-inflammatory states, which if unbalanced can worsen the secondary injury. 111 , 115 , 116 Microglia in the M1 state are pro-inflammatory and can further contribute to secondary injury. 111 , 116 The reduction of butyrate-producing microbes seen after SCI can result in more microglia with the M1 phenotype.…”

Section: Spinal Cord Injurymentioning

confidence: 99%

“…Treatment with FMT from a sham mouse reduces the activated morphology of astrocytes and microglia indicating that ameliorating gut dysbiosis in SCI prevents the overactivation of glia 110 . While glia are important in the response to SCI, there is a delicate balance between pro‐ and anti‐inflammatory states, which if unbalanced can worsen the secondary injury 111,115,116 . Microglia in the M1 state are pro‐inflammatory and can further contribute to secondary injury 111,116 .…”

Section: Spinal Cord Injurymentioning

confidence: 99%

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Gut microbiome and neurosurgery: Implications for treatment

Willman

Reddy

et al. 2022

Clinical and Translational Dis

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Introduction: The aim of this review is to summarize the current understanding of the gut-brain axis (GBA), its impact on neurosurgery, and its implications for future treatment. Background: An abundance of research has established the existence of a collection of pathways between the gut microbiome and the central nervous system (CNS), commonly known as the GBA. Complicating this relationship, the gut microbiome bacterial diversity appears to change with age, antibiotic exposure and a number of external and internal factors. Methods: In this paper, we present the current understanding of the key protective and deleterious roles the gut microbiome plays in the pathogenesis of several common neurosurgical concerns. Results: Specifically, we examine how spinal cord injury, traumatic brain injury and stroke may cause gut microbial dysbiosis. Furthermore, this link appears to be bidirectional as gut dysbiosis contributes to secondary CNS injury in each of these ailment settings. This toxic cycle may be broken, and the future secondary damage rescued by timely, therapeutic, gut microbiome modification. In addition, a robust gut microbiome appears to improve outcomes in brain tumour treatment. There are several primary routes by which microbiome dysbiosis may be ameliorated, including faecal microbiota transplant, oral probiotics, bacteriophages, genetic modification of gut microbiota and vagus nerve stimulation. Conclusion: The GBA represents an important component of patient care in the field of neurosurgery. Future research may illuminate ideal methods of therapeutic microbiome modulation in distinct pathogenic settings.

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Section: Spinal Cord Injurymentioning

confidence: 99%

Section: Spinal Cord Injurymentioning

confidence: 99%

Gut microbiome and neurosurgery: Implications for treatment

Willman

Reddy

et al. 2022

Clinical and Translational Dis

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“…While the scar may inhibit regeneration through the lesion, it also preserves the viable tissue surrounding the lesion [ 67 ]. Glial scar formation results from a combination of complex processes including inflammation, reactive gliosis, apoptosis, autophagy, and others [ 68 , 69 , 70 ]. To design effective therapeutics, the potential consequences of manipulation of each process must be carefully considered.…”

Section: Introductionmentioning

confidence: 99%

Current Advancements in Spinal Cord Injury Research—Glial Scar Formation and Neural Regeneration

Clifford

Finkel

Rodriguez

et al. 2023

Cells

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Spinal cord injury (SCI) is a complex tissue injury resulting in permanent and degenerating damage to the central nervous system (CNS). Detrimental cellular processes occur after SCI, including axonal degeneration, neuronal loss, neuroinflammation, reactive gliosis, and scar formation. The glial scar border forms to segregate the neural lesion and isolate spreading inflammation, reactive oxygen species, and excitotoxicity at the injury epicenter to preserve surrounding healthy tissue. The scar border is a physicochemical barrier composed of elongated astrocytes, fibroblasts, and microglia secreting chondroitin sulfate proteoglycans, collogen, and the dense extra-cellular matrix. While this physiological response preserves viable neural tissue, it is also detrimental to regeneration. To overcome negative outcomes associated with scar formation, therapeutic strategies have been developed: the prevention of scar formation, the resolution of the developed scar, cell transplantation into the lesion, and endogenous cell reprogramming. This review focuses on cellular/molecular aspects of glial scar formation, and discusses advantages and disadvantages of strategies to promote regeneration after SCI.

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“…ECM stiffness also plays a role in cell migration, proliferation, and survival [ 15 ]. Glial cells secrete components of the ECM that have been shown to be modulated following nerve injury [ 16 , 17 ]. From a pathophysiological perspective, peripheral nerve injury promotes an immune and inflammatory response in the central nervous system, which involves the activation of glial cells, which in turn affects the homeostatic balance as a result of changes in neuron–glial interactions.…”

Section: Introductionmentioning

confidence: 99%

“…Parameters such as pulse width, frequency, amplitude, latency period, and active vs. passive recharge can have a differential effect on the neuron–glial environment. Our group reported the modulation of genes related to the neuron–glial network following induction of the SNI model as well as reversed expression changes as a result of treatment with DTMP [ 16 , 17 ]. Proteomic analyses allowed the study of the effect of SCS on pain-related pathways using the SNI model of neuropathic pain.…”

Section: Introductionmentioning

confidence: 99%

Regulation of Expression of Extracellular Matrix Proteins by Differential Target Multiplexed Spinal Cord Stimulation (SCS) and Traditional Low-Rate SCS in a Rat Nerve Injury Model

Tilley

Vallejo

Vetri

et al. 2023

Biology

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There is limited research on the association between the extracellular matrix (ECM) and chronic neuropathic pain. The objective of this study was twofold. Firstly, we aimed to assess changes in expression levels and the phosphorylation of ECM-related proteins due to the spared nerve injury (SNI) model of neuropathic pain. Secondly, two modalities of spinal cord stimulation (SCS) were compared for their ability to reverse the changes induced by the pain model back toward normal, non-injury levels. We identified 186 proteins as ECM-related and as having significant changes in protein expression among at least one of the four experimental groups. Of the two SCS treatments, the differential target multiplexed programming (DTMP) approach reversed expression levels of 83% of proteins affected by the pain model back to levels seen in uninjured animals, whereas a low-rate (LR-SCS) approach reversed 67%. There were 93 ECM-related proteins identified in the phosphoproteomic dataset, having a combined 883 phosphorylated isoforms. DTMP back-regulated 76% of phosphoproteins affected by the pain model back toward levels found in uninjured animals, whereas LR-SCS back-regulated 58%. This study expands our knowledge of ECM-related proteins responding to a neuropathic pain model as well as providing a better perspective on the mechanism of action of SCS therapy.

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The Glial Cells Respond to Spinal Cord Injury

Cited by 15 publications

References 168 publications

Gut microbiome and neurosurgery: Implications for treatment

Gut microbiome and neurosurgery: Implications for treatment

Current Advancements in Spinal Cord Injury Research—Glial Scar Formation and Neural Regeneration

Regulation of Expression of Extracellular Matrix Proteins by Differential Target Multiplexed Spinal Cord Stimulation (SCS) and Traditional Low-Rate SCS in a Rat Nerve Injury Model

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