Evidence map›Paper›PMID 26376826›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2016

Transforming growth factor-β-sphingosine kinase 1/S1P signaling upregulates microRNA-21 to promote fibrosis in renal tubular epithelial cells.

Xiujuan Liu, Quan Hong, Zhen Wang, Yanyan Yu, Xin Zou, Lihong Xu

Open access · greenAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

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  10. Antagonizing S1PInternational journal of molecular sciences · 2021
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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

6 authors at 2 institutions in 1 country.

Xiujuan LiuDepartment of Nephrology, the 94th Hospital of Chinese People's Liberation Army (Changcheng Hospital affiliated to Nanchang University), Nanchang 330002, China xiujuan_liu796@163.com.
Quan HongDepartment of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing 100853, China.
Zhen WangDepartment of Nephrology, the 94th Hospital of Chinese People's Liberation Army (Changcheng Hospital affiliated to Nanchang University), Nanchang 330002, China.
Yanyan YuDepartment of Nephrology, the 94th Hospital of Chinese People's Liberation Army (Changcheng Hospital affiliated to Nanchang University), Nanchang 330002, China.
Xin ZouDepartment of Nephrology, the 94th Hospital of Chinese People's Liberation Army (Changcheng Hospital affiliated to Nanchang University), Nanchang 330002, China.
Lihong XuDepartment of Nephrology, the 94th Hospital of Chinese People's Liberation Army (Changcheng Hospital affiliated to Nanchang University), Nanchang 330002, China.
Nanchang University · CNState Key Laboratory of Kidney Diseases

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal fibrosis is a progressive pathological change characterized by tubular cell apoptosis, tubulointerstitial fibroblast proliferation, and excessive deposition of extracellular matrix (ECM). miR-21 has been implicated in transforming growth factor-β (TGF-β)-stimulated tissue fibrosis. Recent studies showed that sphingosine kinase/sphingosine-1-phosphate (SphK/S1P) are also critical for TGF-β-stimulated tissue fibrosis; however, it is not clear whether SphK/S1P interacts with miR-21 or not. In this study, we hypothesized that SphK/S1P signaling is linked to upregulation of miR-21 by TGF-β. To verify this hypothesis, we first determined that miR-21 was highly expressed in renal tubular epithelial cells (TECs) stimulated with TGF-β by using qRT-PCR and Northern blotting. Simultaneously, inhibition of miR-21, mediated by the corresponding antimir, markedly decreased the expression and deposition of type I collagen, fibronectin (Fn), cysteine-rich protein 61 (CCN1), α-smooth muscle actin, and fibroblast-specific protein1 in TGF-β-treated TECs. ELISA and qRT-PCR were used to measure the S1P and SphK1 levels in TECs. S1P production was induced by TGF-β through activation of SphK1. Furthermore, it was observed that TGF-β-stimulated upregulation of miR-21 was abolished by SphK1 siRNA and was restored by the addition of exogenous S1P. Blocking S1PR2 also inhibited upregulation of miR-21. Additionally, miR-21 overexpression attenuated the repression of TGF-β-stimulated ECM deposition and epithelial-mesenchymal transition by SphK1 and S1PR2 siRNA. In summary, our study demonstrates a link between SphK1/S1P and TGF-β-induced miR-21 in renal TECs and may represent a novel therapeutic target in renal fibrosis.

Indexed as

Signal TransductionBlotting, NorthernCell SurvivalEpithelial CellsHumansLysophospholipidsMicroRNAsPhosphotransferases (Alcohol Group Acceptor)Real-Time Polymerase Chain ReactionSphingosineSphingosine KinaseTransforming Growth Factor betaLysophospholipidsMicroRNAsMIRN21 microRNA, humanPhosphotransferases (Alcohol Group Acceptor)Sphingosinesphingosine 1-phosphateSphingosine KinaseTransforming Growth Factor betamiRNA-21renal fibrosissphingosine-1-phosphatesphingosine kinasetubular epithelial cells

Identifiers

PMID26376826
PMCPMC4935438
OpenAlexW2339107339

What OpenQuestion holds

Textmetadata
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.