Evidence map›Paper›PMID 30394829›Full record

ArticleCell cycle (Georgetown, Tex.)2019

miR-191 secreted by platelet-derived microvesicles induced apoptosis of renal tubular epithelial cells and participated in renal ischemia-reperfusion injury via inhibiting CBS.

Xiao-Qiang Wu, Xiang-Yong Tian, Zhi-Wei Wang, Xuan Wu, Jun-Peng Wang, Tian-Zhong Yan

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 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

6 authors at 2 institutions in 1 country.

Xiao-Qiang Wua Department of Urology, Henan Provincial People's Hospital , People's Hospital of Zhengzhou University , Zhengzhou , China.
Xiang-Yong Tiana Department of Urology, Henan Provincial People's Hospital , People's Hospital of Zhengzhou University , Zhengzhou , China.
Zhi-Wei Wanga Department of Urology, Henan Provincial People's Hospital , People's Hospital of Zhengzhou University , Zhengzhou , China.
Xuan Wua Department of Urology, Henan Provincial People's Hospital , People's Hospital of Zhengzhou University , Zhengzhou , China.
Jun-Peng Wanga Department of Urology, Henan Provincial People's Hospital , People's Hospital of Zhengzhou University , Zhengzhou , China.
Tian-Zhong Yana Department of Urology, Henan Provincial People's Hospital , People's Hospital of Zhengzhou University , Zhengzhou , China.
Henan Provincial People's Hospital · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we aimed to reveal the role of miR-191 in apoptosis of renal tubular epithelial cells and in the involvement of renal ischemia-reperfusion injury. Renal transplantation rat model was established. miR-191 and Cystathionine-β-synthase (CBS) were measured by qRT-PCR and Western blot. The regulation of miR-191 on CBS was detected by luciferase reporter assay. We found miR-191 expression in platelets and platelet microvesicles (P-MVs) of patients and model rats was significantly upregulated than that of health and normal rats. Also, mRNA and protein levels of CBS in renal tissues of patients were significantly downregulated than that of health and normal rats. We also found that P-MVs could transfer miR-191 to HK-2 cells. Luciferase reporter assay showed that CBS was a direct target of miR-191. In addition, we proved that P-MVs-secreted miR-191 inhibited CBS expression in HK-2 cells, and P-MVs-secreted miR-191 promoted HK-2 cell apoptosis via CBS. Finally, we verified the trends of CBS expressions, HK-2 cell apoptosis and apoptosis-related proteins in vivo were similar as the trends in vitro. Therefore, CBS was a direct target of miR-191, and miR-191 could transfer to HK-2 cells via P-MVs to decrease the expression of CBS, thus to promote cell apoptosis and renal IR injury.

Indexed as

ApoptosisAllograftsAnimalsBlood PlateletsCell-Derived MicroparticlesCell LineCystathionine beta-SynthaseDisease Models, AnimalEpithelial CellsGraft RejectionHumansKidney TransplantationKidney TubulesMaleMicroRNAsPrimary Graft DysfunctionCystathionine beta-SynthaseMicroRNAsMIRN191 microRNA, humanCystathionine-β-synthasemiR-191renal ischemia-reperfusion injuryrenal transplantation

Identifiers

PMID30394829
PMCPMC6343735
OpenAlexW2900204516

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.