ArticleAnnals of clinical and translational neurology2021
Mechanism of ARPP21 antagonistic intron miR-128 on neurological function repair after stroke.
Article in Annals of clinical and translational neurology, 2021. 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 It has been retracted, and should not be counted.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 7 papers.
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
7 citing papers in PubMed, 8 citations in OpenAlex.
- Considering Context-Specific microRNAs in Ischemic Stroke with Three "W": Where, When, and What.Molecular neurobiology · 2024Review
- The ability of microRNAs to regulate the immune response in ischemia/reperfusion inflammatory pathways.Genes and immunity · 2024Review
- RNA profiling of human dorsal root ganglia reveals sex differences in mechanisms promoting neuropathic pain.Brain : a journal of neurology · 2023Article
- Multiregion transcriptomic profiling of the primate brain reveals signatures of aging and the social environment.Nature neuroscience · 2022Article
- MicroRNA-582-5p targeting Creb1 modulates apoptosis in cardiomyocytes hypoxia/reperfusion-induced injury.Immunity, inflammation and disease · 2022Article
- miRNA Involvement in Cerebral Ischemia-Reperfusion Injury.Frontiers in neuroscience · 2022Review
- Comprehensive Analysis of Hub Genes Associated With Competing Endogenous RNA Networks in Stroke Using Bioinformatics Analysis.Frontiers in genetics · 2021Article
Corrections and comments
- Retraction · 2024-05-20Author Unresponsive · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Original Data and/or Images not Provided and/or not Available · Plagiarism of Image · Unreliable Data · · see also: https://pubpeer.com/publications/CA9454D2D2A40E807A3B6F12261C2A
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveStroke is a cerebrovascular disorder that often causes neurological function defects. ARPP21 is a conserved host gene of miR-128 controlling neurodevelopmental functions. This study investigated the mechanism of ARPP21 antagonistic intron miR-128 on neurological function repair after stroke.
methodsExpressions of ARPP21 and miR-128 in stroke patients were detected. The mouse neurons and astrocytes were cultured in vitro and treated with oxygen-glucose deprivation (OGD). The OGD-treated cells were transfected with pc-ARPP21 and miR-128 mimic. The proliferation of astrocytes, and the apoptosis of neurons and astrocytes were detected, and inflammatory factors of astrocytes were measured. The binding relationship between miR-128 and CREB1 was verified. The rat model of middle cerebral artery occlusion (MCAO) was established. ARPP21 expression in model rats was detected. The effects of pc-ARPP21 on neuron injury, brain edema volume, and cerebral infarct in rats were observed.
resultsARPP21 expression was downregulated and miR-128 expression was upregulated in stroke patients. pc-ARPP21 facilitated the proliferation of astrocytes and inhibited apoptosis of neurons and astrocytes, and reduced inflammation of astrocytes. miR-128 mimic could reverse these effects of pc-ARPP21 on neurons and astrocytes. miR-128 targeted CREB1 and reduced BDNF secretion. In vitro experiments confirmed that ARPP21 expression was decreased in MCAO rats, and pc-ARPP21 promoted neurological function repair after stroke.
conclusionARPP21 upregulated CREB1 and BDNF expressions by antagonizing miR-128, thus inhibiting neuronal apoptosis and promoting neurological function repair after stroke. This study may offer a novel target for the management of stroke.
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Registered trials
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