Demyelination Initiated by Oligodendrocyte Apoptosis through Enhancing Endoplasmic Reticulum–Mitochondria Interactions and Id2 Expression after Compressed Spinal Cord Injury in Rats

Huang, Si-Qin; Tang, Cheng‐Lin; Sun, Shanquan; Yang, Cheng; Xu, Jin; Wang, Kejian; Lu, WW; Huang, Juan; Zhuo, Fei; Qiu, Guo-Ping; Wu, Xiuyu; Qi, Wei

doi:10.1111/cns.12155

Cited by 35 publications

(30 citation statements)

References 85 publications

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“…In addition to these changes, layers of the myelin sheath were folded, wrinkled, and disorganized, with evidence of demyelinated areas seven days after CSCI. Similarly, other authors [30] found that myelin sheaths became swollen, degenerated and were broken down gradually. In addition, the axolemma was separated from the myelin sheath.…”

Section: Discussionsupporting

confidence: 56%

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Histological, immunohistochemical and ultrastructural study of secondary compressed spinal cord injury in a rat model

Ramadan¹,

Abdel-Hamid²,

Alkarim

et al. 2017

Folia Histochem Cytobiol.

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Introduction. Spinal cord injury (SCI) is a life-disrupting condition in which the first few days are the most critical. Secondary conditions remain the main causes of death for people with SCI. The response of different cell types to SCI and their role at different times in the progression of secondary degeneration are not well understood. The aim of this study was to study the histopathological changes of compressed spinal cord injury (CSCI) in a rat model. Material and methods. Forty adult male Sprague-Dawley rats were divided into four groups. In group I, the rats were left without any surgical intervention (control). In group II, the rats were subjected to laminectomy without spinal cord compression (sham-operated). In group III, the rats were sacrificed one day after CSCI. In group IV, the rats were sacrificed seven days after CSCI. The light microscopy was employed to study the morphology using H&E, osmic acid staining and immunohistochemistry to detect glial fibrillary acidic protein (GFAP). The electron microscopy was applied for ultrastructure study. Results. Histopathological examination of the posterior funiculus of the white matter revealed minute hemorrhages and localized necrotic areas on day 1, which transformed to areas of cavitation and fibrinoid necrosis surrounded by a demarcating rim of numerous astrocytes by day 7. The mean percentage of area of GFAP expression increased significantly by day 7. Osmic acid staining revealed swollen nerve fibers after one day, while numerous fibers had been lost by day 7. An ultrastructure study revealed swollen redundant thinned myelin and myelin splitting, as well as degeneration of axoplasm on day 1. On day 7, layers of the myelin sheath were folded and wrinkled with partial or complete demyelination areas. The myelin lamellae were disorganized and loose. The G-ratio was significantly greater on day 1 than day 7 after CSCI. Conclusions. In the rat model of CSCI details of the progressive spinal cord injury can be analyzed by morphological methods and may be helpful in the identification of the onset and type of clinical intervention.

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Section: Discussionsupporting

confidence: 56%

“…In addition, the axolemma was separated from the myelin sheath. The axoplasm in the lesion area contained varying degrees of reduction in the mitochondria and microtubules [30].…”

Section: Discussionmentioning

confidence: 99%

Histological, immunohistochemical and ultrastructural study of secondary compressed spinal cord injury in a rat model

Ramadan¹,

Abdel-Hamid²,

Alkarim

et al. 2017

Folia Histochem Cytobiol.

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“…ER is responsible for lipid synthesis, protein folding, protein synthesis and intracellular calcium homeostasis. Additionally, there is increasing evidence that ER plays a significant role in the regulation of cell apoptosis, which depends on the intrinsic mitochondria‐mediated death signaling pathway . ER stress induces the expressions of GRP78 and CHOP, which are the ER stress‐related apoptotic factor, and stimulates the unfolded protein response that is closely related with mitochondrial dysfunction .…”

Section: Discussionmentioning

confidence: 99%

Silencing of JMJD2B induces cell apoptosis via mitochondria‐mediated and death receptor‐mediated pathway activation in colorectal cancer

Sun

Wang

et al. 2014

J of Digest Diseases

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“…Subsequently, the sections were immersed in 1% cresyl violet solution for 10 min and quickly dehydrated with 70% and 95% alcohol until myelinated tracts of the spinal columns were stained blue [27]. Three sections per mice were chosen for assessing the myelinated area of spinal white matter.…”

Section: Methodsmentioning

confidence: 99%

G-1 exerts neuroprotective effects through G protein-coupled estrogen receptor 1 following spinal cord injury in mice

et al. 2016

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Spinal cord injury (SCI) always occurs accidently and leads to motor dysfunction because of biochemical and pathological events. Estrogen has been shown to be neuroprotective against SCI through estrogen receptors (ERs), but the underlying mechanisms have not been fully elucidated. In the present study, we investigated the role of a newly found membrane ER, G protein-coupled estrogen receptor 1 (GPR30 or GPER1), and discussed the feasibility of a GPR30 agonist as an estrogen replacement. Forty adult female C57BL/6J mice (10–12 weeks old) were divided randomly into vehicle, G-1, E2, G-1 + G-15 and E2 + G-15 groups. All mice were subjected to SCI using a crushing injury approach. The specific GPR30 agonist, G-1, mimicked the effects of E2 treatment by preventing SCI-induced apoptotic cell death and enhancing motor functional recovery after injury. GPR30 activation regulated phosphatidylinositol 3-kinase (PI3K)/Akt and MAPK/extracellular signal-regulated kinase (ERK) signalling pathways, increased GPR30 and anti-apoptosis proteins Bcl-2 and brain derived neurotrophic factor (BDNF), but decreased the pro-apoptosis factor Bax and cleaved caspase-3. However, the neuroprotective effects of G-1 and E2 were blocked by the specific GPR30 antagonist, G-15. Thus, GPR30 rather than classic ERs is required to induce estrogenic neuroprotective effects. Given that estrogen replacement therapy may cause unexpected side effects, especially on the reproductive system, GPR30 agonists may represent a potential therapeutic approach for treating SCI.

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Demyelination Initiated by Oligodendrocyte Apoptosis through Enhancing Endoplasmic Reticulum–Mitochondria Interactions and Id2 Expression after Compressed Spinal Cord Injury in Rats

Abstract: Demyelination occurred after CSCI and might be partly caused by oligodendrocyte apoptosis, which was positively correlated with ER-mitochondria interactions and enhanced Id2 expression after CSCI in rats.

Cited by 35 publications

References 85 publications

Histological, immunohistochemical and ultrastructural study of secondary compressed spinal cord injury in a rat model

Histological, immunohistochemical and ultrastructural study of secondary compressed spinal cord injury in a rat model

Silencing of JMJD2B induces cell apoptosis via mitochondria‐mediated and death receptor‐mediated pathway activation in colorectal cancer

G-1 exerts neuroprotective effects through G protein-coupled estrogen receptor 1 following spinal cord injury in mice

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