Evidence map›Paper›PMID 30240403›Full record

ArticlePloS one2018

An enriched environment prevents diabetes-induced cognitive impairment in rats by enhancing exosomal miR-146a secretion from endogenous bone marrow-derived mesenchymal stem cells.

Kenta Kubota, Masako Nakano, Eiji Kobayashi, Yuka Mizue, Takako Chikenji, Miho Otani, Kanna Nagaishi, Mineko Fujimiya

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 75 citations in OpenAlex.

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  17. A state-of-the-art review on miRNA in prevention and treatment of AlzheimerZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023
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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

8 authors at 1 institution in 1 country.

Kenta KubotaDepartment of Anatomy, Sapporo Medical University, School of Medicine, Sapporo, Hokkaido, Japan.ORCID 0000-0003-1176-1991
Masako NakanoDepartment of Anatomy, Sapporo Medical University, School of Medicine, Sapporo, Hokkaido, Japan.
Eiji KobayashiDepartment of Anatomy, Sapporo Medical University, School of Medicine, Sapporo, Hokkaido, Japan.
Yuka MizueDepartment of Anatomy, Sapporo Medical University, School of Medicine, Sapporo, Hokkaido, Japan.
Takako ChikenjiDepartment of Anatomy, Sapporo Medical University, School of Medicine, Sapporo, Hokkaido, Japan.
Miho OtaniDepartment of Anatomy, Sapporo Medical University, School of Medicine, Sapporo, Hokkaido, Japan.
Kanna NagaishiDepartment of Anatomy, Sapporo Medical University, School of Medicine, Sapporo, Hokkaido, Japan.
Mineko FujimiyaDepartment of Anatomy, Sapporo Medical University, School of Medicine, Sapporo, Hokkaido, Japan.
Sapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence suggests that an enriched environment (EE) ameliorates cognitive impairment by promoting repair of brain damage. However, the mechanisms by which this occurs have not been determined. To address this issue, we investigated whether an EE enhanced the capability of endogenous bone marrow-derived mesenchymal stem/stromal cells (BM-MSCs) to prevent hippocampal damage due to diabetes by focusing on miRNA carried in BM-MSC-derived exosomes. In diabetic streptozotocin (STZ) rats housed in an EE (STZ/EE), cognitive impairment was significantly reduced, and both neuronal and astroglial damage in the hippocampus was alleviated compared with STZ rats housed in conventional cages (STZ/CC). BM-MSCs isolated from STZ/CC rats had functional and morphological abnormalities that were not detected in STZ/EE BM-MSCs. The miR-146a levels in exosomes in conditioned medium of cultured BM-MSCs and serum from STZ/CC rats were decreased compared with non-diabetic rats, and the level was restored in STZ/EE rats. Thus, the data suggest that increased levels of miR-146a in sera were derived from endogenous BM-MSCs in STZ/EE rats. To examine the possibility that increased miR-146a in serum may exert anti-inflammatory effects on astrocytes in diabetic rats, astrocytes transfected with miR-146a were stimulated with advanced glycation end products (AGEs) to mimic diabetic conditions. The expression of IRAK1, NF-κB, and tumor necrosis factor-α was significantly higher in AGE-stimulated astrocytes, and these factors were decreased in miR-146a-transfected astrocytes. These results suggested that EEs stimulate up-regulation of exosomal miR-146a secretion by endogenous BM-MSCs, which exerts anti-inflammatory effects on damaged astrocytes and prevents diabetes-induced cognitive impairment.

Indexed as

AnimalsAstrocytesBone Marrow CellsCA1 Region, HippocampalCells, CulturedCognitive DysfunctionDiabetes Mellitus, ExperimentalExosomesGlycation End Products, AdvancedInterleukin-1 Receptor-Associated KinasesMaleMaze LearningMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMicroRNAsOxidative StressGlycation End Products, AdvancedInterleukin-1 Receptor-Associated KinasesIRAK1 protein, ratMicroRNAsMIRN146a microRNA, ratTumor Necrosis Factor-alpha

Identifiers

PMID30240403
PMCPMC6150479
OpenAlexW2890938599

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.