Evidence mapPaperPMID 37167274Full record

ArticleAmerican journal of physiology. Renal physiology2023

The miR-143/145 cluster induced by TGF-β1 suppresses Wilms' tumor 1 expression in cultured human podocytes.

Akifumi Tabei, Toru Sakairi, Hiroko Hamatani, Yuko Ohishi, Mitsuharu Watanabe, Masao Nakasatomi, Hidekazu Ikeuchi, Yoriaki Kaneko, Jeffrey B Kopp, Keiju Hiromura

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

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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

10 authors at 2 institutions in 2 countries.

Akifumi TabeiDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Gunma, Japan.
Toru SakairiDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Gunma, Japan.ORCID 0000-0003-2804-485X
Hiroko HamataniDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Gunma, Japan.ORCID 0000-0001-7727-6986
Yuko OhishiDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Gunma, Japan.
Mitsuharu WatanabeDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Gunma, Japan.
Masao NakasatomiDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Gunma, Japan.
Hidekazu IkeuchiDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Gunma, Japan.ORCID 0000-0002-0768-7090
Yoriaki KanekoDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Gunma, Japan.
Jeffrey B KoppKidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States.ORCID 0000-0001-9052-186X
Keiju HiromuraDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Gunma, Japan.ORCID 0000-0002-9490-8364
Gunma University · JPNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor (TGF)-β1 contributes to podocyte injury in various glomerular diseases, including diabetic kidney disease, probably at least in part by attenuating the expression of Wilms' tumor 1 (WT1). However, the precise mechanisms remain to be defined. We performed miRNA microarray analysis in a human podocyte cell line cultured with TGF-β1 to examine the roles of miRNAs in podocyte damage. The microarray analysis identified miR-143-3p as the miRNA with the greatest increase following exposure to TGF-β1. Quantitative RT-PCR confirmed a significant increase in the miR-143-3p/145-5p cluster in TGF-β1-supplemented cultured podocytes and demonstrated upregulation of miR-143-3p in the glomeruli of mice with type 2 diabetes. Ectopic expression of miR-143-3p and miR-145-5p suppressed WT1 expression in cultured podocytes. Furthermore, inhibition of Smad or mammalian target of rapamycin signaling each partially reversed the TGF-β1-induced increase in miR-143-3p/145-5p and decrease in WT1. In conclusion, TGF-β1 induces expression of miR-143-3p/145-5p in part through Smad and mammalian target of rapamycin pathways, and miR-143-3p/145-5p reduces expression of WT1 in cultured human podocytes. miR-143-3p/145-5p may contribute to TGF-β1-induced podocyte injury.

Indexed as

Diabetes Mellitus, Type 2Diabetic NephropathiesMicroRNAsPodocytesTransforming Growth Factor beta1AnimalsHumansMiceTOR Serine-Threonine KinasesWT1 ProteinsMicroRNAsMIRN143 microRNA, humanMIRN145 microRNA, humanTOR Serine-Threonine KinasesTransforming Growth Factor beta1WT1 protein, humanWT1 Proteinsdiabetic kidney diseasemiR-143/miR-145podocytetransforming growth factor-β1Wilms’ tumor 1

Identifiers

PMID37167274
PMCPMC10511167
OpenAlexW4376226446

What Socratic holds

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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 Socratic graph.