Both endoplasmic reticulum and mitochondrial pathways are involved in oligodendrocyte apoptosis induced by capsular hemorrhage

Zhuo, Fei; Qiu, Guo-Ping; Xu, Jin; Yang, Mei; Wang, Kejian; Liu, Hui; Huang, Juan; Lu, WW; Liu, Qian; Xu, Shan; Huang, Si-Qin; Sun, Shanquan

doi:10.1016/j.mcn.2016.01.009

Cited by 20 publications

(18 citation statements)

References 50 publications

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“…[101][102][103] As the cell type that contains a high level of iron in the CNS, oligodendrocytes are very sensitive to iron overload 104 and thus particularly susceptible to ICH injury. It has been reported that ICH induces oligodendrocyte death and demyelination in white matter, 105,106 where functional and morphological maintenance is highly dependent on oligodendrocytes and their myelin sheaths. 107 How do oligodendrocytes die after ICH?…”

Section: Oligodendrocyte Death After Ichmentioning

confidence: 99%

Oligodendrocytes in intracerebral hemorrhage

Kang

Yao

2019

CNS Neurosci Ther

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Intracerebral hemorrhage (ICH) is a cerebrovascular disorder with high mortality and disability rates. Although a lot of effort has been put in ICH, there is still no effective treatment for this devastating disease. Recent studies suggest that oligodendrocytes play an important role in brain repair after ICH and thus may be targeted for the therapies of ICH. Here in this review, we first introduce the origin, migration, proliferation, differentiation, and myelination of oligodendrocytes under physiological condition. Second, recent findings on how ICH affects oligodendrocyte biology and function are reviewed. Third, potential crosstalk between oligodendrocytes and other cells in the brain is also summarized. Last, we discuss the therapeutic potential of oligodendrocyte‐based treatments in ICH. Our goal is to provide a comprehensive review on the biology and function of oligodendrocytes under both physiological and ICH conditions.

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Section: Oligodendrocyte Death After Ichmentioning

confidence: 99%

Oligodendrocytes in intracerebral hemorrhage

Kang

Yao

2019

CNS Neurosci Ther

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“…Hypertensive ICH could lead to demyelination and downregulation of MBP expression in the white matter. Morphologic changes of myelin sheaths included swelling and damage at first, followed by demyelination and lastly oligodendrocyte apoptosis after ICH [30]. Accompanying this, a large number of pathological molecules were highly expressed or overactivated, such as TNF- α [31], RIPK1 [32], receptor for advanced glycation end-products (RAGE), HMGB1 [33], CD47 [34], SC1 [35], β -APP [36], and JNK signaling pathway [37].…”

Section: White Matter Injury After Hypertensive Ichmentioning

confidence: 99%

“…The pathological changes of white matter after hypertensive ICH could be quickly and accurately found by immunohistochemical staining, western blotting, southern blotting, PCR, and so forth [29, 30, 33]. The pathological changes of white matter after hypertensive ICH were involved not only in morphology, but also in function.…”

Section: White Matter Injury After Hypertensive Ichmentioning

confidence: 99%

White Matter Injury and Recovery after Hypertensive Intracerebral Hemorrhage

Zuo

Pan

Qiang

et al. 2017

BioMed Research International

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Hypertensive intracerebral hemorrhage (ICH) could very probably trigger white matter injury in patients. Through the continuous study of white matter injury after hypertensive ICH, we achieve a more profound understanding of the pathophysiological mechanism of its occurrence and development. At the same time, we found a series of drugs and treatment methods for the white matter repair. In the current reality, the research paradigm of white matter injury after hypertensive ICH is relatively obsolete or incomplete, and there are still lots of deficiencies in the research. In the face of the profound changes of stroke research perspective, we believe that the combination of the lenticulostriate artery, nerve nuclei of the hypothalamus-thalamus-basal ganglia, and the white matter fibers located within the capsula interna will be beneficial to the research of white matter injury and repair. This paper has classified and analyzed the study of white matter injury and repair after hypertensive ICH and also rethought the shortcomings of the current research. We hope that it could help researchers further explore and study white matter injury and repair after hypertensive ICH.

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“…17) Injury of axonal tracts involves demyelination process as well as the destruction of axonal fibers. In a recent study, Zhuo et al 18) addressed the mechanisms of demyelination in rats that received autologous blood injection into the area adjacent to the internal capsule. Under their experimental conditions, demyelination was observed progressively between 1 and 7 d after blood injection, as revealed by the ultrastructural changes in myelinated nerve fibers as well as the decrease of myelin basic protein.…”

Section: Mechanisms and Potential Therapeutic Interventionsmentioning

confidence: 99%

“…Concurrently, apoptosis of myelin-forming oligodendrocytes was observed as activation of caspase-3 in this cell population. Caspase-3 activation can be initiated by several pathways, and Zhuo et al 18) observed both activation of caspase-12 (that may represent the involvement of endoplasmic reticulum stress) and release of cytochrome c (that represents activation of mitochondrial apoptotic pathway).…”

Section: Mechanisms and Potential Therapeutic Interventionsmentioning

confidence: 99%

Intracerebral Hemorrhage as an Axonal Tract Injury Disorder with Inflammatory Reactions

Katsuki

2017

Biological & Pharmaceutical Bulletin

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Intracerebral hemorrhage (ICH) is a neurological disorder frequently accompanied by severe dysfunction. Critical pathogenic events leading to poor prognosis should be identified for the development of novel effective therapies for ICH. Here we focus on the injury of the axonal tract, particularly of the internal capsule, with reference to its contribution to ICH pathology and potential therapeutic interventions in addition to its cellular mechanisms. Studies on human ICH patients and rodent models of ICH suggest that invasion of hematoma into the internal capsule greatly worsens the severity of post-ICH symptoms. A blood-derived protease thrombin may play an important role in the acute phase of axonal tract injury in the internal capsule that includes compromised axonal transport and fragmentation of axonal structures. Several agents such as clioquinol, melatonin and Am80 (a retinoic acid receptor agonist) have been shown to produce therapeutic effects on rodent models of ICH associated with injury of the internal capsule. In the course of examinations on the effect of Am80, we obtained evidence for the involvement of CXCL2, a neutrophil chemotactic factor, in the pathogenesis of ICH. Accordingly, we also refer to the potential roles of infiltrating neutrophils and inflammatory responses in axonal tract injury and resultant neurological dysfunction in ICH.

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Both endoplasmic reticulum and mitochondrial pathways are involved in oligodendrocyte apoptosis induced by capsular hemorrhage

Cited by 20 publications

References 50 publications

Oligodendrocytes in intracerebral hemorrhage

Oligodendrocytes in intracerebral hemorrhage

White Matter Injury and Recovery after Hypertensive Intracerebral Hemorrhage

Intracerebral Hemorrhage as an Axonal Tract Injury Disorder with Inflammatory Reactions

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