Early ultrastructural changes after brief histotoxic hypoxia in cultured cortical and hippocampal CA1 neurons

Dux, E.; Oschlies, U.; Uto, Akira; Kusumoto, M.; Hossmann, Konstantin‐Alexander

doi:10.1007/s004010050559

Cited by 13 publications

(4 citation statements)

References 26 publications

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“…Generally, the structural integrity of the Golgi apparatus is maintained by complicated mechanisms and disturbances often result in Golgi fragmentation (Marsh and Howell, 2002), which is involved in many neurodegenerative diseases incuding Alzheimer’s disease (Gonatas et al, 2006), stroke or hypoxia-related brain injury (Dux et al, 1996; Hayashi and Abe, 2004). Until now, the potential interaction between PPARs and fragmentation of the Golgi apparatus is poorly understood (de Figueiredo and Brown, 1999).…”

Section: Discussionmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptor δ Regulation of miR-15a in Ischemia-Induced Cerebral Vascular Endothelial Injury

et al. 2010

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Cerebral vascular endothelial cell (CEC) degeneration significantly contributes to blood-brain barrier (BBB) breakdown and neuronal loss after cerebral ischemia. Recently, emerging data suggest that peroxisome proliferator-activated receptor ␦ (PPAR␦) activation has a potential neuroprotective role in ischemic stroke. Here we report for the first time that PPAR␦ is significantly reduced in oxygen-glucose deprivation (

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Section: Discussionmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptor δ Regulation of miR-15a in Ischemia-Induced Cerebral Vascular Endothelial Injury

et al. 2010

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“…However, the mechanism and function of this phenomenon are not clear. Nevertheless, it is undoubtedly true that the disaggregation of ribosomes is one of the first pathological alterations that heralds neuronal death . Thereby, we determined that, when the concentration of Mn 2+ was between 25 and 50 m m , some organelles (including ribosome and mitochondria) were damaged in RGCs.…”

Section: Discussionmentioning

confidence: 89%

Manganese‐enhanced MRI optic nerve tracking: effect of intravitreal manganese dose on retinal toxicity

Luo

Liu

et al. 2012

NMR in Biomedicine

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The aim of this study was to provide data on the dose dependence of manganese-enhanced MRI (MEMRI) in the visual pathway of experimental rats and to study the toxicity of MnCl₂ to the retina. Sprague-Dawley rats were intravitreally injected with 2 μL of 0, 10, 25, 50, 75, 100, 150 and 300 mM MnCl₂, respectively. The contrast-to-noise ratio (CNR) of MEMRI for optic nerve enhancement was measured at different concentrations of MnCl₂. Simultaneously, the toxicity of manganese was evaluated by counting retinal ganglion cells and by retinal histological examination using light microscopy and transmission electron microscopy. The CNR increased with increasing concentration of MnCl₂ up to 75 mM. Retinal ganglion cell densities were reduced significantly when the concentration of MnCl₂ in the intravitreal injection was equal to or greater than 75 mM. Increasing numbers of ribosomes in retinal ganglion cells were first detected at 25 mM of MnCl₂. The retinal toxicity of MnCl₂ at higher concentration also included mitochondrial pathology and cell disruption of retinal ganglion cells, as well as abnormalities of photoreceptor and retinal pigment epithelium cells. It can be concluded that intravitreal injection of MnCl₂ induces retinal cell damage that appears to start from 25 mM. The concentration of MnCl₂ should not exceed 25 mm through intravitreal injection for visual pathway MEMRI in the rat.

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“…Accumulated ubiquinated protein clusters convert to insoluble, toxic protein aggregates (PAs) . Mitochondria and endoplasmic reticulum (ER) swell and alterations in their ability to undergo fusion/fission have been noted . Mitochondria can lose their electrical potential and become dysfunctional .…”

Section: Delayed Neuronal Deathmentioning

confidence: 99%

Regulation of mRNA following brain ischemia and reperfusion

DeGracia

2017

WIREs RNA

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There is growing appreciation that mRNA regulation plays important roles in disease and injury. mRNA regulation and ribonomics occur in brain ischemia and reperfusion (I/R) following stroke and cardiac arrest and resuscitation. It was recognized over 40 years ago that translation arrest (TA) accompanies brain I/R and is now recognized as part of the intrinsic stress responses triggered in neurons. However, neuron death correlates to a prolonged TA in cells fated to undergo delayed neuronal death (DND). Dysfunction of mRNA regulatory processes in cells fated to DND prevents them from translating stress-induced mRNAs such as heat shock proteins. The morphological and biochemical studies of mRNA regulation in postischemic neurons are discussed in the context of the large variety of molecular damage induced by ischemic injury. Open issues and areas of future investigation are highlighted. A sober look at the molecular complexity of ischemia-induced neuronal injury suggests that a network framework will assist in making sense of this complexity. The ribonomic network sits between the gene network and the various protein and metabolic networks. Thus, targeting the ribonomic network may prove more effective at neuroprotection than targeting specific molecular pathways, for which all efforts have failed to the present time to stop DND in stroke and after cardiac arrest. WIREs RNA 2017, 8:e1415. doi: 10.1002/wrna.1415 For further resources related to this article, please visit the WIREs website.

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Early ultrastructural changes after brief histotoxic hypoxia in cultured cortical and hippocampal CA1 neurons

Cited by 13 publications

References 26 publications

Peroxisome Proliferator-Activated Receptor δ Regulation of miR-15a in Ischemia-Induced Cerebral Vascular Endothelial Injury

Peroxisome Proliferator-Activated Receptor δ Regulation of miR-15a in Ischemia-Induced Cerebral Vascular Endothelial Injury

Manganese‐enhanced MRI optic nerve tracking: effect of intravitreal manganese dose on retinal toxicity

Regulation of mRNA following brain ischemia and reperfusion

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