Electron microscopic study of the progeny of ependymal stem cells in the normal and injured spinal cord

Attar, Ayhan; Kaptanoğlu, Erkan; Aydin, Zafer; Ayten, Murat; Sargon, Mustafa F.

doi:10.1016/j.surneu.2005.07.057

Cited by 13 publications

(2 citation statements)

References 17 publications

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“…The mechanisms behind the plasticity of ependymal cells and their migration [51] appear to be a response to the mechanical and inflammatory damage and can result in trans-differentiation of ependymal cells into astrocytes [51], oligodendrocytes [52] and neural progenitors [53]. The importance of this plasticity includes an active support and guidance provided to regenerating axons [17,38,54].…”

Section: Discussionmentioning

confidence: 99%

Prolonged inflammation leads to ongoing damage after spinal cord injury

et al. 2020

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The pathogenesis of spinal cord injury (SCI) remains poorly understood and treatment remains limited. Emerging evidence indicates that post-SCI inflammation is severe but the role of reactive astrogliosis not well understood given its implication in ongoing inflammation as damaging or neuroprotective. We have completed an extensive systematic study with MRI, histopathology, proteomics and ELISA analyses designed to further define the severe protracted and damaging inflammation after SCI in a rat model. We have identified 3 distinct phases of SCI: acute (first 2 days), inflammatory (starting day 3) and resolution (>3 months) in 16 weeks follow up. Actively phagocytizing, CD68 + /CD163macrophages infiltrate myelin-rich necrotic areas converting them into cavities of injury (COI) when deep in the spinal cord. Alternatively, superficial SCI areas are infiltrated by granulomatous tissue, or arachnoiditis where glial cells are obliterated. In the COI, CD68+/CD163macrophage numbers reach a maximum in the first 4 weeks and then decline. Myelin phagocytosis is present at 16 weeks indicating ongoing inflammatory damage. The COI and arachnoiditis are defined by a wall of progressively hypertrophied astrocytes. MR imaging indicates persistent spinal cord edema that is linked to the severity of inflammation. Microhemorrhages in the spinal cord around the lesion are eliminated, presumably by reactive astrocytes within the first week post-injury. Acutely increased levels of TNF-alpha, IL-1beta, IFN-gamma and other proinflammatory cytokines, chemokines and proteases decrease and anti-inflammatory cytokines increase in later phases. In this study we elucidated a number of fundamental mechanisms in pathogenesis of SCI and have demonstrated a close association between progressive astrogliosis and reduction in the severity of inflammation.

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Section: Discussionmentioning

confidence: 99%

Prolonged inflammation leads to ongoing damage after spinal cord injury

et al. 2020

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“…The mechanisms behind the plasticity of ependymal cells and their migration [49] appear to be a response to the mechanical and inflammatory damage and can result in trans-differentiation of ependymal cells into astrocytes [49], oligodendrocytes 50 and neural progenitors [51]. The importance of this plasticity includes an active support and guidance provided to regenerating axons [15,36,52].…”

Section: Discussionmentioning

confidence: 99%

Prolonged inflammation leads to ongoing damage after spinal cord injury

Kwiecień

Dąbrowski

Dąbrowska–Bouta³

et al. 2019

Preprint

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27The pathogenesis of spinal cord injury (SCI) remains poorly understood and treatment remains 28 limited. Emerging evidence indicates the severity of post-SCI inflammation and an ongoing 29 controversy in the roles of astrocytes with studies identifying astrocytes as associated both with 30 ongoing inflammation and damage as well as potentially having a protective role. We have 31 completed an extensive systematic study with MRI, histopathology, proteomics and ELISA 32 analyses designed to further define the severe protracted and damaging inflammation after SCI in 33 a rat model. We have identified 3 distinct phases of SCI: acute (first 2 days), inflammatory (starting 34 day 3) and resolution (>3 months) in 16 weeks follow up. Actively phagocytizing, CD68 + /CD163 -35 macrophages infiltrate myelin-rich necrotic areas converting them into cavities of injury (COI) 36 when deep in the spinal cord. Alternatively, superficial SCI areas are infiltrated by granulomatous 37 tissue, or arachnoiditis where glial cells are obliterated. In the COI, CD68+/CD163macrophage 38 numbers reach a maximum in the first 4 weeks and then decline. Myelin phagocytosis is present 39 at 16 weeks indicating ongoing inflammatory damage. The COI and arachnoiditis are defined by 40 a wall of progressively hypertrophied astrocytes. MR imaging indicates persistent spinal cord 41 edema that is linked to the severity of inflammation. Microhemorrhages in the spinal cord around 42 the lesion are eliminated, presumably by reactive astrocytes within the first week post-injury. 43Acutely increased levels of TNF-, IL-1, IFN- and other pro-inflammatory cytokines, 44 chemokines and proteases decrease and anti-inflammatory cytokines increase in later phases. In 45 this study we elucidated a number of fundamental mechanisms in pathogenesis of SCI and have 46 demonstrated a close association between progressive astrogliosis and reduction in the severity of 47 inflammation. 48 4 49 50 KEYWORDS 51 Neurotrauma inflammation, cavity of injury, arachnoiditis, M1 macrophage, astrogliosis. 5 52 53Spinal cord injury (SCI) is a leading cause of long term morbidity after motor vehicle 54 accidents or trauma in combat, with no clinically standardized or substantially effective treatment. 55Effective therapeutics have remained limited due to an incomplete understanding of the 56 pathogenesis of SCI and thus identified effective therapeutic targets while the underlying and 57 persistent inflammatory damage after SCI remains poorly characterized. The role of invasive 58 inflammatory cells and specifically astrogliosis in the ongoing damage after SCI is not fully 59 defined with studies supporting both a role in SCI damage [1,2] as well as a proposed potential 60 protective role for astrocytes [3]. We have completed an extensive analysis with MRI, 61 histochemistry, proteomics and ELISA in a rat model of SCI in order to further define the 62 pathological changes that occur after SCI. 63 SCI initiates hemorrhage and ischemia, free radical release, severe inflammation,...

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Veterinary Aspects

Rusbridge

2014

Syringomyelia

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Syringomyelia is an increasingly common diagnosis in veterinary medicine, especially in toy breed dogs where selections for small size and brachycephalic head shape are contributing factors. The most common cause is a condition analogous to Chiari I malformation in humans. This chapter details the pathophysiology, clinical signs, medical and surgical management, progression and prognosis of the canine condition. As a naturally occurring model of both syringomyelia and central neuropathic pain, observations that may have relevance to understanding of the pathophysiology of Chiari malformation and syringomyelia in humans are discussed. Finally, current knowledge of genetic factors and breeding advice is reviewed

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Electron microscopic study of the progeny of ependymal stem cells in the normal and injured spinal cord

Cited by 13 publications

References 17 publications

Prolonged inflammation leads to ongoing damage after spinal cord injury

Prolonged inflammation leads to ongoing damage after spinal cord injury

Prolonged inflammation leads to ongoing damage after spinal cord injury

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