ArticleFrontiers in cellular neuroscience2020
RNA Binding Protein Motif 3 Inhibits Oxygen-Glucose Deprivation/Reoxygenation-Induced Apoptosis Through Promoting Stress Granules Formation in PC12 Cells and Rat Primary Cortical Neurons.
Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 29 citations in OpenAlex.
- Loss of O-GlcNAc transferase activity impairs the dynamic formation of protective stress granules in ischemic cardiomyocytes.The Biochemical journal · 2026Article
- Harpagide attenuates cerebral ischemic injury by modulating mitochondrial calcium homeostasis associated with the AMPK-MCU axis.Scientific reports · 2026Article
- The Role of Stress Granules in Cardiovascular Diseases.Reviews in cardiovascular medicine · 2026Review
- Augmenting the Endogenous RBM3 Response Protects Against Burn-Induced Acute Kidney Injury by Enhancing Macrophage-Mediated Resolution of Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- TIA1-mediated stress granules inhibit the neuroinflammation and neurodegeneration after spinal cord injury through LCN2 signaling.Cellular and molecular life sciences : CMLS · 2026Article
- Stress Granules: Novel Regulators of Programmed Cell Death.Mini reviews in medicinal chemistry · 2026Review
- Targeting G3BP1 Condensate Topology Promotes Stress Granule Assembly via mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Human RBM3 protein is prone to form neuronal aggregates opposed by the proteasome.Biology open · 2026Article
- Procyanidin B3 and Its Derivatives Alleviate Neuronal Injury by Targeting G3BP1 for Ischemic Stroke Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Unveiling the Spatiotemporal dynamics of stress granule phase transition: A key mechanism governing neuronal fate in acute ischemic stroke.Molecular biology reports · 2025Review
- Stress granules and cell death: crosstalk and potential therapeutic strategies in infectious diseases.Cell death & disease · 2025Review
- Therapeutic modulation of protein RBM3 for ischemic stroke treatment.Frontiers in pharmacology · 2025Review
- Article
- Analysis of different expression RNA binding protein genes in mouse microglia cell from the brains of mice 72 h after subarachnoid hemorrhage or sham operation.BMC medical genomics · 2024Article
- Mechanism of Dcp2/RNCR3/Dkc1/Snora62 axis regulating neuronal apoptosis in chronic cerebral ischemia.Cell biology and toxicology · 2023Article
- Mild Therapeutic Hypothermia and Putative Mechanisms of Hair Cell Survival in the Cochlea.Antioxidants & redox signaling · 2022Article
- Stress Granules and Acute Ischemic Stroke: Beyond mRNA Translation.International journal of molecular sciences · 2022Review
- Candesartan Reduces Neuronal Apoptosis Caused by Ischemic Stroke via Regulating the FFAR1/ITGA4 Pathway.Mediators of inflammation · 2022Article
- Identification of a 6-RBP gene signature for a comprehensive analysis of glioma and ischemic stroke: Cognitive impairment and aging-related hypoxic stress.Frontiers in aging neuroscience · 2022Article
- Cooling and Sterile Inflammation in an Oxygen-Glucose-Deprivation/Reperfusion Injury Model in BV-2 Microglia.Mediators of inflammation · 2021Article
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9 authors at 2 institutions in 1 country.
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Abstract
As a sensitive cold-shock protein, RNA binding protein motif 3 (RBM3) exhibits a neuroprotective function in the condition of brain injury. However, how RBM3 is involved in acute ischemic stroke by affecting stress granules (SGs) remains unclear. Here, we established an oxygen-glucose deprivation/reperfusion (OGD/R) model in rat primary cortical neurons and PC12 cells to explore the potential mechanism between RBM3 and SG formation in acute ischemic/reperfusion (I/R) condition. The immunofluorescence results showed that the SG formation significantly decreased in rat primary cortical neurons and PC12 cells during the reperfusion period after 6 h of OGD stimulation. The western blot results, flow cytometry analysis, and cell viability assessment showed that the RBM3 expression and ratio of cell viability significantly decreased, while the rate of apoptosis increased in PC12 cells during the reperfusion period after 6 h of OGD stimulation. Co-immunoprecipitation (Co-IP) and immunofluorescence indicated that RBM3 and GTPase-activating protein-binding protein 1 (G3BP1) colocalized cytoplasm of PC12 cells after 6 h of OGD stimulation when the SGs formation reached the highest level. Besides, overexpression and knockdown of the RBM3 were achieved via plasmid transfection and CRISPR-Cas9 technology, respectively. The results of overexpression and knockdown of RBM3 gene illustrated the pivotal role of RBM3 in affecting SG formation and apoptosis level in OGD-treated PC12 cells. In conclusion, RBM3 could combine with G3BP1 resulted in increasing stress granules generation in rat primary cortical neurons and PC12 cells after 6 h of oxygen-glucose deprivation (OGD) injury, which ultimately reduced the apoptosis in OGD-induced cells. Our study may enable a new promising target for alleviating ischemia-reperfusion injury in cells.
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