Evidence map›Paper›PMID 26134897›Full record

ArticleInternational journal of molecular medicine2015

miR-135 family members mediate podocyte injury through the activation of Wnt/β-catenin signaling.

Xianggui Yang, Xiaoyan Wang, Fang Nie, Tianming Liu, Xuejing Yu, Honglian Wang, Qianyin Li, Rui Peng, Zhaomin Mao, Qin Zhou and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  8. Article
  9. Coronavirus Disease (COVID)-19 and Diabetic Kidney Disease.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
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  15. Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019
    Review
  16. Article
  17. Article
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  19. Article
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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

11 authors at 3 institutions in 1 country.

Xianggui YangDivision of Molecular Nephrology and Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, P.R. China.
Xiaoyan WangDivision of Molecular Nephrology and Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, P.R. China.
Fang NieDivision of Molecular Nephrology and Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, P.R. China.
Tianming LiuDivision of Molecular Nephrology and Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, P.R. China.
Xuejing YuDepartment of Cardiology, The Fifth Medical College, Peking University, Beijing, P.R. China.
Honglian WangResearch Center of Combined Traditional Chinese and Western Medicine, The Affiliated Traditional Medicine Hospital, Luzhou Medical College, Luzhou, Sichuan, P.R. China.
Qianyin LiDivision of Molecular Nephrology and Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, P.R. China.
Rui PengDivision of Molecular Nephrology and Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, P.R. China.
Zhaomin MaoDivision of Molecular Nephrology and Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, P.R. China.
Qin ZhouDivision of Molecular Nephrology and Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, P.R. China.
Ge LiDivision of Molecular Nephrology and Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, P.R. China.
Chongqing Medical University · CNPeking University · CNSouthwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The upregulation of Wnt/β-catenin signaling occurs in virtually all types of kidney disease and is associated with podocyte injury. However, the precise mechanisms involved in the development of kidney disease remain to be elucidated. MicroRNAs (miRNAs or miRs) are a class of short non-coding RNAs and they have been shown to be regulators of gene expression, mainly by binding to the untranslated region (UTR) of mRNAs. The aim of the present study was to determine the role of the 2 members of the miR-135 family (miR‑135a and miR‑135b) in podocyte injury and to elucidate the mechanisms responsible for the damage to podocytes. The results revealed that miR-135a and miR-135b were upregulated in models of podocyte injury and in glomeruli isolated from patients with focal segmental glomerulosclerosis (FSGS). The ectopic expression of miR-135a and miR‑135b led to severe podocyte injury and the disorder of the podocyte cytoskeleton. Our findings demonstrated that miR-135a and miR‑135b activated Wnt/β‑catenin signaling and induced the nuclear translocation of β-catenin. Using luciferase reporter assays, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis, glycogen synthase kinase 3β (GSK3β) was identified as a target gene of miR-135a and miR‑135b. To the best of our knowledge, this is the first study to demonstrate that members of the miR-135 family (specifically miR-135a and miR‑135b) regulate the expression of GSK3β, thus playing a role in the development of podocyte injury and the disorder of the podocyte cytoskeleton. This is an important finding as it may contribute to the development of novel therapeutics for podocyte injury-associated glomerulopathies.

Indexed as

Up-RegulationWnt Signaling PathwayAnimalsCell LineDown-RegulationGlomerulosclerosis, Focal SegmentalGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansMice, Inbred BALB CMicroRNAsPodocytesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseMicroRNAsMIRN135 microRNA, humanMirn135 microRNA, mouse

Identifiers

PMID26134897
PMCPMC4533775
OpenAlexW2124847465

What OpenQuestion holds

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LicenceCC BY
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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.