Evidence map›Paper›PMID 33568779›Full record

ArticleCommunications biology2021

Inhibition of miR-96-5p in the mouse brain increases glutathione levels by altering NOVA1 expression.

Chisato Kinoshita, Kazue Kikuchi-Utsumi, Koji Aoyama, Ryo Suzuki, Yayoi Okamoto, Nobuko Matsumura, Daiki Omata, Kazuo Maruyama, Toshio Nakaki

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Glutathione in HIV-Associated Neurocognitive Disorders.Current issues in molecular biology · 2024
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Glutathione in the Brain.International journal of molecular sciences · 2021
    Review
  12. The Role of Non-Coding RNAs in the Neuroprotective Effects of Glutathione.International journal of molecular sciences · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Chisato KinoshitaDepartment of Pharmacology, Teikyo University School of Medicine, Tokyo, Japan.ORCID 0000-0001-5877-0196
Kazue Kikuchi-UtsumiDepartment of Pharmacology, Teikyo University School of Medicine, Tokyo, Japan.
Koji AoyamaDepartment of Pharmacology, Teikyo University School of Medicine, Tokyo, Japan.
Ryo SuzukiLaboratory of Drug and Gene Delivery, Faculty of Pharma-Science, Teikyo University, Tokyo, Japan.
Yayoi OkamotoDepartment of Pharmacology, Teikyo University School of Medicine, Tokyo, Japan.
Nobuko MatsumuraDepartment of Pharmacology, Teikyo University School of Medicine, Tokyo, Japan.
Daiki OmataLaboratory of Drug and Gene Delivery, Faculty of Pharma-Science, Teikyo University, Tokyo, Japan.
Kazuo MaruyamaLaboratory of Theranostics, Faculty of Pharma-Science, Teikyo University, Tokyo, Japan.
Toshio NakakiDepartment of Pharmacology, Teikyo University School of Medicine, Tokyo, Japan. nakaki@med.teikyo-u.ac.jp.
Teikyo University · JPTeikyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutathione (GSH) is an important antioxidant that plays a critical role in neuroprotection. GSH depletion in neurons induces oxidative stress and thereby promotes neuronal damage, which in turn is regarded as a hallmark of the early stage of neurodegenerative diseases. The neuronal GSH level is mainly regulated by cysteine transporter EAAC1 and its inhibitor, GTRAP3-18. In this study, we found that the GTRAP3-18 level was increased by up-regulation of the microRNA miR-96-5p, which was found to decrease EAAC1 levels in our previous study. Since the 3'-UTR region of GTRAP3-18 lacks the consensus sequence for miR-96-5p, an unidentified protein should be responsible for the intermediate regulation of GTRAP3-18 expression by miR-96-5p. Here, we discovered that RNA-binding protein NOVA1 functions as an intermediate protein for GTRAP3-18 expression via miR-96-5p. Moreover, we show that intra-arterial injection of a miR-96-5p-inhibiting nucleic acid to living mice by a drug delivery system using microbubbles and ultrasound decreased the level of GTRAP3-18 via NOVA1 and increased the levels of EAAC1 and GSH in the dentate gyrus of the hippocampus. These findings suggest that the delivery of a miR-96-5p inhibitor to the brain would efficiently increase the neuroprotective activity by increasing GSH levels via EAAC1, GTRAP3-18 and NOVA1.

Indexed as

AnimalsCell Line, TumorDentate GyrusExcitatory Amino Acid Transporter 3GlutathioneHeat-Shock ProteinsHEK293 CellsHumansInjections, Intra-ArterialMaleMembrane Transport ProteinsMiceMice, Inbred C57BLMicrobubblesMicroRNAsNeuro-Oncological Ventral AntigenArl6ip5 protein, mouseExcitatory Amino Acid Transporter 3GlutathioneHeat-Shock ProteinsMembrane Transport ProteinsMicroRNAsMirn96 microRNA, mouseNeuro-Oncological Ventral AntigenNeuroprotective AgentsNova1 protein, mouseRNA-Binding ProteinsSlc1a1 protein, mouse

Identifiers

PMID33568779
PMCPMC7876013
OpenAlexW3127935696

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Registered trials

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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.