ArticleFrontiers in neuroscience2018
Neuroprotective Effect of Protein Phosphatase 2A/Tristetraprolin Following Subarachnoid Hemorrhage in Rats.
Article in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- A Systematic Review of Inflammatory Cytokine Changes Following Aneurysmal Subarachnoid Hemorrhage in Animal Models and Humans.Translational stroke research · 2022Pooled it
- Sphingosine-1-phosphate Signalling in Aneurysmal Subarachnoid Haemorrhage: Basic Science to Clinical Translation.Translational stroke research · 2024Review
- Cross-disease transcriptomic analysis reveals DOK3 and PAPOLA as therapeutic targets for neuroinflammatory and tumorigenic processes.Frontiers in immunology · 2024Article
- Clinical Potential of Immunotherapies in Subarachnoid Hemorrhage Treatment: Mechanistic Dissection of Innate and Adaptive Immune Responses.Aging and disease · 2023Review
- Molecular Pharmacology and Novel Potential Therapeutic Applications of Fingolimod.Frontiers in pharmacology · 2022Review
- Potential of Amantadine to Ameliorate Glutamate-Induced Pyramidal Cells Toxicity in Juvenile Rat' Brain Cortex.Neurotoxicity research · 2021Article
- Neuroprotective Strategies in Aneurysmal Subarachnoid Hemorrhage (aSAH).International journal of molecular sciences · 2021Review
- Targeting Tristetraprolin Expression or Functional Activity Regulates Inflammatory Response Induced by MSU Crystals.Frontiers in immunology · 2021Article
- Tristetraprolin attenuates brain edema in a rat model of cerebral hemorrhage.Brain and behavior · 2019Article
- c‑Jun N‑terminal kinase inhibition attenuates early brain injury induced neuronal apoptosis via decreasing p53 phosphorylation and mitochondrial apoptotic pathway activation in subarachnoid hemorrhage rats.Molecular medicine reports · 2019Article
Corrections and comments
- Retraction · 2024-07-18Concerns/Issues about Data · Concerns/Issues about Image · Investigation by Journal/Publisher · Original Data and/or Images not Provided and/or not Available · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early brain injury (EBI) following subarachnoid hemorrhage (SAH) can lead to inflammation and neuronal dysfunction. There is a need for effective strategies to mitigate these effects and improve the outcome of patients who experience SAH. The mRNA-destabilizing protein tristetraprolin (TTP) is an anti-inflammatory factor that induces the decay of cytokine transcripts and has been implicated in diseases such as glioma. However, the mechanism of action of TTP in EBI after SAH is unclear. The present study investigated the effects of TTP regulation via phosphorylation in a rat model of SAH by protein phosphatase (PP)2A, which is a pleiotropic enzyme complex with multiple substrate phospho-proteins. We hypothesized that inhibitory phosphorylation of TTP by PP2A would reduce neuroinflammation and apoptosis. To evaluate the function of each factor, the PP2A agonist FTY720, short interfering (si)RNAs targeting TTP and PP2A were administered to rats by intracerebroventricular injection 24 h before SAH. Rats were evaluated with SAH grade, neurological score, brain water content and by western blotting, and terminal deoxynucleotidyltransferase dUTP nick-end labeling. We found that endogenous PP2A and TTP levels were increased after SAH. FTY720 induced PP2A activation would lead to dephosphorylation and activation of TTP and decreased production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8. SiRNA-mediated TTP knockdown abolished anti-inflammatory effects of FTY720 treatment, indicating that PP2A was associated with TTP activation
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.