ArticleCellular and molecular neurobiology2012
Ischaemia-induced protein ubiquitinylation is differentially accompanied with heat-shock protein 70 expression after naïve and preconditioned ischaemia.
Article in Cellular and molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Involvement of Proteasomal and Endoplasmic Reticulum Stress in Neurodegeneration After Global Brain Ischemia.Molecular neurobiology · 2023Article
- Neuroprotective effects and mechanisms of ischemic/hypoxic preconditioning on neurological diseases.CNS neuroscience & therapeutics · 2021Review
- Proteasome Stress Triggers Death of SH-SY5Y and T98G Cells via Different Cellular Mechanisms.Neurochemical research · 2017Article
- Short Chemical Ischemia Triggers Phosphorylation of eIF2α and Death of SH-SY5Y Cells but not Proteasome Stress and Heat Shock Protein Response in both SH-SY5Y and T98G Cells.Journal of molecular neuroscience : MN · 2016Article
- Possible contribution of proteins of Bcl-2 family in neuronal death following transient global brain ischemia.Cellular and molecular neurobiology · 2015Article
- Oxygen glucose deprivation post-conditioning protects cortical neurons against oxygen-glucose deprivation injury: role of HSP70 and inhibition of apoptosis.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2014Article
- An Immunological Approach to Increase the Brain's Resilience to Insults.ISRN neuroscience · 2014Article
- Ischemia-induced inhibition of mitochondrial complex I in rat brain: effect of permeabilization method and electron acceptor.Neurochemical research · 2012Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the effect of transient global brain ischaemia, both naïve and preconditioned, on accumulation of ubiquitinylated proteins and induction of stress/chaperone proteins specific to cytoplasm and endoplasmic reticulum. In addition, possible correlation between stress response and ischaemia/induced translocation of p53 to mitochondria was investigated. Rats were subjected to 15-min forebrain ischaemia followed by 1, 3, 24 and 72 h of reperfusion. Transient cerebral ischaemia induced a massive increase in protein ubiquitinylation in the hippocampus as well as in both cerebral and cerebellar cortex. Enhanced ubiquitinylation of proteins was paralleled with transcriptional activation of hsp70.1 gene but not hsp70.3 gene. However, HSP70 protein level was significantly elevated 24 and 72 h after ischaemia. Neither ischaemia nor ischaemia followed by reperfusion was associated with significant changes of GRP78, GADD34 and GADD153 levels. Ubiquitinylated protein level was elevated 1 and 48 h after sub-lethal 5 min ischaemia. Preconditioned ischaemia (15 min ischaemia followed 48 h after sub-lethal ischaemia) was associated with even enhanced accumulation of ubiquitinylated proteins of molecular mass higher than 110 kDa. HSP70 protein was significantly elevated 48 h after sub-lethal ischaemia as well as after preconditioned ischaemia and all investigated time intervals of reperfusion. The elevated level of HSP70 might represent plausible explanation of inhibition of both translocation of p53 to mitochondria and ischaemia-induced apoptosis observed after preconditioned ischaemia.
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