ArticleAmerican journal of translational research2020
Up-regulation of miR-137 can inhibit PTN in target manner to regulate PTN/PTPRZ pathway to prevent cognitive dysfunction caused by propofol.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Literature-derived serum miRNA signatures associated with cognitive decline in Alzheimer's disease: integrated analysis and machine learning-based diagnostic modeling.Alzheimer's research & therapy · 2026Article
- The Role of miR-137 in Neurodegenerative Disorders.International journal of molecular sciences · 2024Review
- Article
- miR-137: A therapeutic candidate or a key molecular regulator in Alzheimer's disease?Journal of Alzheimer's disease reportsReview
Corrections and comments
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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
objectiveTo explore the effects of miR-137 on cognitive dysfunction in rats induced by propofol (PRO).
methodsMale SD rats and SK-N-SH cells were purchased, and control and PRO groups were set up in the rats, and the same groups were set up in the cells. On the basis of the PRO group, miR-137 and PTN were up-regulated or down-regulated, and cognitive dysfunction and cell biological functions in each group were detected.
resultsThe cognitive function of rats induced by PRO might be affected. We observed that the escape latency of PRO group was significantly prolonged, with significantly lower percentage of time for target platform exploration and times of crossing the platform, while over-expression of miR-137 or knock down of PTN could change the above results. Under PRO intervention, the expression of miR-137 in SK-N-SH cells decreased in a dose-dependent manner, while the expression and protein level of PTN in SK-N-SH cells increased in a dose-dependent manner. Cytotoxicity test yielded a 30 μM concentration of PRO as the optimal experimental concentration. When miR-137 and PTN were up-regulated or down-regulated, PRO-induced cell apoptosis, proliferation and PTN/PTPRZ pathway protein phosphorylation level were effectively reversed. Dual luciferase reporter confirmed that miR-137 and PTN have targeted relationship.
conclusionUp-regulation of miR-137 can at least partially regulate PTN/PTPRZ pathway through the inhibition of PTN in a targeted manner, effectively inhibit cell apoptosis, and protect cognitive dysfunction caused by PRO.
Indexed as
Identifiers
33312384PMC7724353W3112261261What OpenQuestion holds
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 OpenQuestion graph.