ArticleInternational journal of molecular medicine2019
miR‑335 promotes stress granule formation to inhibit apoptosis by targeting ROCK2 in acute ischemic stroke.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Delaying Stress Granule Disassembly by PARG Inhibition Attenuates Renal Tubular Cell Pyroptosis in Acute Kidney Injury.International journal of molecular sciences · 2026Article
- The Role of Stress Granules in Cardiovascular Diseases.Reviews in cardiovascular medicine · 2026Review
- Stress Granules: Novel Regulators of Programmed Cell Death.Mini reviews in medicinal chemistry · 2026Review
- Crosstalk Between Signaling Stroke Cascade and Therapeutic Receptors PPAR-γ, ROCK, CB1R, and CB2R: From Mechanism to Therapies.Translational stroke research · 2025Review
- Unveiling the Spatiotemporal dynamics of stress granule phase transition: A key mechanism governing neuronal fate in acute ischemic stroke.Molecular biology reports · 2025Review
- DDX3X/MAVS alleviates doxorubicin‑induced cardiotoxicity by regulating stress granules.Molecular medicine reports · 2025Article
- Connecting the Dots: Stress Granule and Cardiovascular Diseases.Journal of cardiovascular translational research · 2025Review
- Identification of potential biomarkers and drug of ischemic stroke in patients with COVID-19 through machine learning.Heliyon · 2024Article
- Review
- MicroRNA-335-5p suppresses voltage-gated sodium channel expression and may be a target for seizure control.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Challenging Cellular Homeostasis: Spatial and Temporal Regulation of miRNAs.International journal of molecular sciences · 2022Review
- MiR-665 Participates in the Protective Effect of Dexmedetomidine in Ischemic Stroke by ROCK2/NF-κB Axis.Neurochemical research · 2022Article
- MiR-335 promotes corneal neovascularization by Targeting EGFR.BMC ophthalmology · 2022Article
- Stress Granules and Acute Ischemic Stroke: Beyond mRNA Translation.International journal of molecular sciences · 2022Review
- SARS-CoV-2 causes a significant stress response mediated by small RNAs in the blood of COVID-19 patients.Molecular therapy. Nucleic acids · 2022Article
- Long non-coding RNA NBAT1, TUG1, miRNA-335, and miRNA-21 as potential biomarkers for acute ischemic stroke and their possible correlation to thyroid hormones.Frontiers in molecular biosciences · 2022Article
- Rho/ROCK Pathway and Noncoding RNAs: Implications in Ischemic Stroke and Spinal Cord Injury.International journal of molecular sciences · 2021Review
- Knockdown of XIST Attenuates Cerebral Ischemia/Reperfusion Injury Through Regulation of miR-362/ROCK2 Axis.Neurochemical research · 2021Article
- Review
- ΜicroRNA-122 protects against ischemic stroke by targeting Maf1.Experimental and therapeutic medicine · 2021Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Under harmful environmental conditions, stress granules (SGs), macromolecular aggregates that are associated with cell survival and death, are produced in the eukaryotic cytoplasm. However, whether and how microRNAs (miRNAs/miRs) modulate SG formation induced by acute ischemic stroke has not been investigated. In the present study, a rat model of middle cerebral artery occlusion (MCAO) was utilized and miRNA array profiling and reverse transcription‑quantitative polymerase chain reaction were performed. The results revealed that miR‑335 was downregulated during acute ischemic stroke, which was concomitant with reduced SG formation, enhanced apoptosis levels and increased Rho associated protein kinase 2 (ROCK2) expression. In the MCAO rat and serum‑free cell models, miR‑335 treatment upregulated SG formation, alleviated the ischemia‑induced infarction, and decreased ROCK2 protein expression and apoptosis levels. By contrast, when compared with miR‑335 treatment, the inhibition of miR‑335 resulted in reduced SG formation and higher ROCK2 expression and apoptosis levels. Target prediction analysis and luciferase 3'‑untranslated region reporter assay identified ROCK2 as the direct target of miR‑335. Furthermore, ROCK2 silencing enhanced SG formation and attenuated the level of apoptosis in the serum‑free cell model. In addition, ROCK2 silencing markedly inhibited the effect of miR‑335 on SG formation and apoptosis levels. Unexpectedly, the phosphorylation of T‑cell intracellular antigen‑1 was significantly inhibited by miR‑335 in the MCAO rat model, which provides a reasonable explanation for the promotional effect of miR‑335 on SG formation by specifically targeting ROCK2. In conclusion, these results demonstrate that miR‑335 promotes SG formation and inhibits apoptosis by reducing ROCK2 expression in acute ischemic stroke, which provides a possible therapeutic target for brain injury.
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