The temporal and spatial dynamics of glyoxalase I following excitoxicity and brain ischaemia

Pieroh, Philipp; Birkenmeier, Gerd; Dehghani, Faramarz

doi:10.1042/bst20140022

Cited by 4 publications

(1 citation statement)

References 48 publications

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“…Glo-1 expression was also shown to be modulated in ischemia. Indeed, following permanent middle cerebral artery occlusion, temporal and spatial changes in Glo-1 immunoreactivity in endothelial cells, neurons and astrocytes were observed (Pieroh et al, 2014 ).…”

Section: Glyoxalase System In Brain Disordersmentioning

confidence: 99%

Methylglyoxal, the dark side of glycolysis

2015

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Glucose is the main energy substrate for the brain. There is now extensive evidence indicating that the metabolic profile of neural cells with regard to glucose utilization and glycolysis rate is not homogenous, with a marked propensity for glycolytic glucose processing in astrocytes compared to neurons. Methylglyoxal, a highly reactive dicarbonyl compound, is inevitably formed as a by-product of glycolysis. Methylglyoxal is a major cell-permeant precursor of advanced glycation end-products (AGEs), which are associated with several pathologies including diabetes, aging and neurodegenerative diseases. In normal situations, cells are protected against methylglyoxal toxicity by different mechanisms and in particular the glyoxalase system, which represents the most important pathway for the detoxification of methylglyoxal. While the neurotoxic effects of methylglyoxal and AGEs are well characterized, our understanding the glyoxalase system in the brain is more scattered. Considering the high energy requirements (i.e., glucose) of the brain, one should expect that the cerebral glyoxalase system is adequately fitted to handle methylglyoxal toxicity. This review focuses on our actual knowledge on the cellular aspects of the glyoxalase system in brain cells, in particular with regard to its activity in astrocytes and neurons. A main emerging concept is that these two neural cell types have different and energetically adapted glyoxalase defense mechanisms which may serve as protective mechanism against methylglyoxal-induced cellular damage.

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Section: Glyoxalase System In Brain Disordersmentioning

confidence: 99%

Methylglyoxal, the dark side of glycolysis

2015

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Comparative Examination of Temporal Glyoxalase 1 Variations Following Perforant Pathway Transection, Excitotoxicity, and Controlled Cortical Impact Injury

et al. 2017

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Following acute neuronal lesions, metabolic imbalance occurs, the rate of glycolysis increases, and methylglyoxal (MGO) forms, finally leading to metabolic dysfunction and inflammation. The glyoxalase system is the main detoxification system for MGO and is impaired following excitotoxicity and stroke. However, it is not known yet whether alterations of the glyoxalase system are also characteristic for other neuronal damage models. Neuronal damage was induced in organotypic hippocampal slice cultures by transection of perforant pathway (PPT; 5 min to 72 h) and N-methyl-D-aspartate (NMDA; 50 μM for 4 h) or in vivo after controlled cortical impact (CCI) injury (2 h to 14 days). Temporal and spatial changes of glyoxalase I (GLO1) were investigated by Western blot analyses and immunohistochemistry. In immunoblot, the GLO1 protein content was not significantly affected by PPT at all investigated time points. As described previously, NMDA treatment led to a GLO1 increase 24 and 48 h after the lesion, whereas PPT increased GLO1 immunoreactivity within neurons only at 48 h postinjury. Immunohistochemistry of brain tissue subjected to CCI unveiled positive GLO1 immunoreactivity in neurons and astrocytes at 1 and 3 days after injury. Two hours and 14 days after CCI, no GLO1 immunoreactivity was observed. GLO1 protein content changes are associated with excitotoxicity but seemingly not to fiber transection. Cell-specific changes in GLO1 immunoreactivity after different in vitro and in vivo lesion types might be a common phenomenon in the aftermath of neuronal lesions.

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Overexpressing glyoxalase 1 attenuates acute hyperglycemia–exacerbated neurological deficits of ischemic stroke in mice

Yang

Sheu

et al. 2023

Translational Research

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The temporal and spatial dynamics of glyoxalase I following excitoxicity and brain ischaemia

Cited by 4 publications

References 48 publications

Methylglyoxal, the dark side of glycolysis

Methylglyoxal, the dark side of glycolysis

Comparative Examination of Temporal Glyoxalase 1 Variations Following Perforant Pathway Transection, Excitotoxicity, and Controlled Cortical Impact Injury

Overexpressing glyoxalase 1 attenuates acute hyperglycemia–exacerbated neurological deficits of ischemic stroke in mice

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