Evidence map›Paper›PMID 28252009›Full record

ArticleScientific reports2017

Nicotine facilitates VSMC dysfunction through a miR-200b/RhoGDIA/cytoskeleton module.

Dongli Liang, Zhaoxia Wang, Zhiqiang Yan, Shangwei Hou, Wangjie Xu, Lianyun Wang, Meisheng Shang, Zhongdong Qiao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Apolipoprotein (a)/Lipoprotein(a)-Induced Oxidative-InflammatoryOxidative medicine and cellular longevity · 2022
    Article
  6. Article
  7. Article
  8. Nicotine and vascular dysfunction.Acta physiologica (Oxford, England) · 2021
    Review
  9. Article
  10. Review
  11. 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

8 authors at 4 institutions in 1 country.

Dongli LiangSchool of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, PR China.
Zhaoxia WangLaboratory Animal Center of Instrumental Analysis Center, Shanghai Jiao Tong University, Shanghai, 200240, PR China.
Zhiqiang YanCentral laboratory, Shanghai Jiao Tong University affiliated Sixth People's Hospital South Campus, Shanghai, 201400, PR China.
Shangwei HouHongqiao international institute of medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200336, PR China.
Wangjie XuSchool of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, PR China.
Lianyun WangSchool of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, PR China.
Meisheng ShangBeijing Anzhen Hospital, Capital Medical University, Beijing, 100029, PR China.
Zhongdong QiaoSchool of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, PR China.
Shanghai Jiao Tong University · CNCapital Medical University · CNShanghai Sixth People's Hospital · CNTongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nicotine can induce the abnormal migration and proliferation of vascular smooth muscle cells (VSMCs). We have previously shown that cytoskeletal proteins and RhoGDIA, a negative regulator of the Rho GTPase pathway, are involved in the nicotine-induced dysfunction of VSMCs. Here, we found that nicotine can activate the Rho GTPase pathway and induce the synthesis of the cytoskeletal proteins in VSMCs through the activation of intracellular downstream signaling pathways, including targets such as MYPT1, PAK1 and PI3K/AKT. Upon nicotine treatment, the mRNA level of RhoGDIA is increased but protein level is decreased both in vitro and in vivo, which suggested a mechanism of post-translational regulation. By the dual luciferase reporter assay, we identified the microRNA-200b (miR-200b) as a modulator of the behavioural changes of VSMCs in response to nicotine through targeting RhoGDIA directly. Introducing miR-200b inhibitors into cultured VSMCs significantly attenuated cell proliferation and migration. Additionally, we found that hypomethylation in the CpG island shore region of miR-200b was responsible for the nicotine-induced miR-200b up-regulation in VSMCs. The study demonstrates that nicotine facilitates VSMC dysfunction through a miR-200b/RhoGDIA/cytoskeleton module through the hypomethylation of miR-200b promoter and suggests that epigenetic modifications may play an important role in the pathological progression.

Indexed as

3' Untranslated RegionsAnimalsBase SequenceCell MovementCell ProliferationCells, CulturedCytoskeletonGanglionic StimulantsGene Expression RegulationHeLa CellsHumansMaleMice, Inbred C57BLMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth Muscle3' Untranslated RegionsGanglionic StimulantsMicroRNAsMirn200 microRNA, mouseNicotinerho Guanine Nucleotide Dissociation Inhibitor alpha

Identifiers

PMID28252009
PMCPMC5333142
OpenAlexW2592659574

What OpenQuestion holds

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LicenceCC BY
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.