ArticleCellular and molecular neurobiology2015
Possible contribution of proteins of Bcl-2 family in neuronal death following transient global brain ischemia.
Article in Cellular and molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 28 citations in OpenAlex.
- Involvement of Proteasomal and Endoplasmic Reticulum Stress in Neurodegeneration After Global Brain Ischemia.Molecular neurobiology · 2023Article
- Blood-Brain Barrier Rescue by Roflumilast After Transient Global Cerebral Ischemia in Rats.Neurotoxicity research · 2023Article
- miR‑183‑5p attenuates cerebral ischemia injury by negatively regulating PTEN.Molecular medicine reports · 2020Article
- Global brain ischemia in rats is associated with mitochondrial release and downregulation of Mfn2 in the cerebral cortex, but not the hippocampus.International journal of molecular medicine · 2019Article
- Cannabinoid Receptor Type 1 Agonist ACEA Improves Cognitive Deficit on STZ-Induced Neurotoxicity Through Apoptosis Pathway and NO Modulation.Neurotoxicity research · 2019Article
- Histone Hyperacetylation as a Response to Global Brain Ischemia Associated with Hyperhomocysteinemia in Rats.International journal of molecular sciences · 2018Article
- MicroRNA-140-5p elevates cerebral protection of dexmedetomidine against hypoxic-ischaemic brain damage via the Wnt/β-catenin signalling pathway.Journal of cellular and molecular medicine · 2018Article
- Inhibition of breast cancer cell growth by theOncology letters · 2017Article
- Proteasome Stress Triggers Death of SH-SY5Y and T98G Cells via Different Cellular Mechanisms.Neurochemical research · 2017Article
- Atorvastatin Attenuates Ischemia/Reperfusion-Induced Hippocampal Neurons Injury Via Akt-nNOS-JNK Signaling Pathway.Cellular and molecular neurobiology · 2017Article
- Iron Loading Selectively Increases Hippocampal Levels of Ubiquitinated Proteins and Impairs Hippocampus-Dependent Memory.Molecular neurobiology · 2016Article
- Pro-apoptotic Action of Corticosterone in Hippocampal Organotypic Cultures.Neurotoxicity research · 2016Article
- Mitochondrial Cyclophilin D as a Potential Therapeutic Target for Ischemia-Induced Facial Palsy in Rats.Cellular and molecular neurobiology · 2015Article
- Cardiac Arrest Alters Regional Ubiquitin Levels in Association with the Blood-Brain Barrier Breakdown and Neuronal Damages in the Porcine Brain.Molecular neurobiology · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteins of Bcl-2 family are crucial regulators of intrinsic (mitochondrial) pathway of apoptosis that is implicated among the mechanisms of ischemic neuronal death. Initiation of mitochondrial apoptosis depends on changes of equilibrium between anti-apoptotic and pro-apoptotic proteins of Bcl-2 family as well as on translocation of pro-apoptotic proteins of Bcl-2 family to mitochondria. The aim of this work was to study the effect of transient global brain ischemia on expression and intracellular distribution of proteins of Bcl-2 family in relation to the ischemia-induced changes of ERK and Akt kinase pathways as well as disturbances in ubiquitin proteasome system. Using four vessel occlusion model of transient global brain ischemia, we have shown that both ischemia in duration of 15 min and the same ischemia followed by 1, 3, 24, and 72 h of reperfusion did not affect the levels of either pro-apoptotic (Bad, PUMA, Bim, Bax, Noxa) or anti-apoptotic (Bcl-2, Bcl-xl, Mcl-1) proteins of Bcl-2 family in total cell extracts from rat hippocampus. However, significantly elevated level of Bad protein in the mitochondria isolated from rat hippocampus was observed already 1 h after ischemia and remained elevated 3 and 24 h after ischemia. We did not observe significant changes of the levels of Puma, Bax, Bcl-2, and Bcl-xl in the mitochondria after ischemia and ischemia followed by reperfusion. Our results might indicate possible involvement of Bad translocation to mitochondria in the mechanisms of neuronal death following transient global brain ischemia.
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