ArticleThe Journal of biological chemistry2016
Stress Granule Induction after Brain Ischemia Is Independent of Eukaryotic Translation Initiation Factor (eIF) 2α Phosphorylation and Is Correlated with a Decrease in eIF4B and eIF4E Proteins.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Loss of O-GlcNAc transferase activity impairs the dynamic formation of protective stress granules in ischemic cardiomyocytes.The Biochemical journal · 2026Article
- Proteomic Analysis of Mouse Cerebral Cortex Following Experimental Ischemic Stroke: Identifying Novel Biomarkers of Damage and Repair.Cellular and molecular neurobiology · 2025Article
- Unveiling the Spatiotemporal dynamics of stress granule phase transition: A key mechanism governing neuronal fate in acute ischemic stroke.Molecular biology reports · 2025Review
- Article
- Hypoxia-induced mitochondrial stress granules.Cell death & disease · 2023Article
- Review
- Preclinical Characterization of Antioxidant Quinolyl Nitrone QN23 as a New Candidate for the Treatment of Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2022Article
- RBM20Journal of molecular and cellular cardiology · 2022Article
- Pathophysiology of stress granules: An emerging link to diseases (Review).International journal of molecular medicine · 2022Review
- Stress Granules and Acute Ischemic Stroke: Beyond mRNA Translation.International journal of molecular sciences · 2022Review
- Phosphorylation of Eukaryotic Initiation Factor 4G1 (eIF4G1) at Ser1147 Is Specific for eIF4G1 Bound to eIF4E in Delayed Neuronal Death after Ischemia.International journal of molecular sciences · 2022Article
- The Integral Role of RNA in Stress Granule Formation and Function.Frontiers in cell and developmental biology · 2021Review
- Characterization of a CholesteroNitrone (ISQ-201), a Novel Drug Candidate for the Treatment of Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2020Article
- Understanding the roles of stress granule during chemotherapy for patients with malignant tumors.American journal of cancer research · 2020Review
- Repeat-associated non-AUG (RAN) translation mechanisms are running into focus for GGGGCC-repeat associated ALS/FTD.Progress in neurobiology · 2019Review
- Stress granule: A promising target for cancer treatment.British journal of pharmacology · 2019Review
- Shared genes between Alzheimer's disease and ischemic stroke.CNS neuroscience & therapeutics · 2019Article
- Stress granules are formed in renal proximal tubular cells during metabolic stress and ischemic injury for cell survival.American journal of physiology. Renal physiology · 2019Article
- Disease of mRNA Regulation: Relevance for Ischemic Brain Injury.Translational stroke research · 2018Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress granules (SGs) are cytoplasmic ribonucleoprotein aggregates that are directly connected with the translation initiation arrest response to cellular stresses. Translation inhibition (TI) is observed in transient brain ischemia, a condition that induces persistent TI even after reperfusion, i.e. when blood flow is restored, and causes delayed neuronal death (DND) in selective vulnerable regions. We previously described a connection between TI and DND in the hippocampal cornu ammonis 1 (CA1) in an animal model of transient brain ischemia. To link the formation of SGs to TI and DND after brain ischemia, we investigated SG induction in brain regions with differential vulnerabilities to ischemia-reperfusion (IR) in this animal model. SG formation is triggered by both eukaryotic translation initiation factor (eIF) 2α phosphorylation and eIF4F complex dysfunction. We analyzed SGs by immunofluorescence colocalization of granule-associated protein T-cell internal antigen-1 with eIF3b, eIF4E, and ribosomal protein S6 and studied eIF2 and eIF4F complex. The results showed that IR stress induced SG formation in the CA1 region after 3-day reperfusion, consistent with TI and DND in CA1. SGs were formed independently of eIF2α phosphorylation, and their appearance was correlated with a decrease in the levels of eIF4F compounds, the cap-binding protein eIF4E, and eIF4B, suggesting that remodeling of the eIF4F complex was required for SG formation. Finally, pharmacological protection of CA1 ischemic neurons with cycloheximide decreased the formation of SGs and restored eIF4E and eIF4B levels in CA1. These findings link changes in eIF4B and eIF4E to SG induction in regions vulnerable to death after IR.
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