Evidence map›Paper›PMID 29100354›Full record

ArticleOncotarget2017

Mechanism of genistein regulating the differentiation of vascular smooth muscle cells into osteoblasts via the OPG/RANKL pathway.

Cheng Shen, Ye Yuan, Fuping Li, Yijie Hu, Yi Song, Shulin Zhao, Qianjin Zhong

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Sialidase Deficiency inFrontiers in cellular and infection microbiology · 2018
    Article
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

7 authors at 2 institutions in 1 country.

Cheng Shen *Department of Cardiovascular Surgery, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, China.
Ye Yuan *Department of Cardiovascular Surgery, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, China.
Fuping LiDepartment of Cardiovascular Surgery, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, China.
Yijie HuDepartment of Cardiovascular Surgery, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, China.
Yi SongDepartment of Cardiovascular Surgery, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, China.
Shulin ZhaoDepartment of Cardiovascular Surgery, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, China.
Qianjin ZhongDepartment of Cardiovascular Surgery, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, China.
Army Medical University · CNDaping Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe present study aimed to investigate the mechanism of genistein, a tyrosine kinase inhibitor, regulating the differentiation of vascular smooth muscle cells (VSMCs) into osteoblasts via the OPG/RANKL (Osteoprotegerin/Receptor Activator of Nuclear Factor-κB Ligand) pathway.

methodsThe mouse VSMCs were isolated, purified and cultured. We constructed the LV5-Tnfrsf11b overexpression lentiviral vector and LV3-OPG-309 interference lentiviral vector. The OPG overexpression was induced and the growth of VSMCs infected with the lentiviral vector was observed. The VSMC calcification and control group were treated with different doses of genistein. The mRNA and protein expression levels of OPG, α-SM-actin (smooth muscle actin), ALP (alkaline phosphatase) and OPN (osteopontin) were detected in VSMCs after treatment using RT-PCR and Western Blot.

resultWe induced OPG overexpression and performed lentiviral vector infection of the VSMCs to suppress OPG expression, respectively, which was followed by treatment with genistein. The results showed that the relative expression of OPG was the highest in the VSMC calcification +genistein +OPG overexpression-inducing treatment group. It was the lowest in the VSMC calcification +OPG expression-suppressing treatment group. The relative expression of ALP was the highest in the VSMC calcification +OPG expression-suppressing treatment group, and the lowest in the VSMCs+genistein treatment group.

conclusionOPG gene plays an important regulatory role in the growth of VSMCs, by suppressing the calcification of VSMCs. Genistein could regulate the differentiation of VSMCs into osteoblasts via the OPG/RANKL pathway in a dose-dependent manner.

Indexed as

genisteinOPG/RANKL pathwayVSMCs

Identifiers

PMID29100354
PMCPMC5652748
OpenAlexW2743830835

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.