Evidence map›Paper›PMID 30372567›Full record

ArticleStem cells (Dayton, Ohio)2019

Glycoprotein M6B Interacts with TβRI to Activate TGF-β-Smad2/3 Signaling and Promote Smooth Muscle Cell Differentiation.

Xiaomeng Zhang, Huaning Xie, Pan Chang, Huishou Zhao, Yunlong Xia, Ling Zhang, Xiong Guo, Chong Huang, Feng Yan, Lang Hu and 8 more

Open access · greenAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Transcriptome Sequencing of LYPLA1 Gene Overexpression and Interference.Animals : an open access journal from MDPI · 2026
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  17. Gasotransmitters: Potential Therapeutic Molecules of Fibrotic Diseases.Oxidative medicine and cellular longevity · 2021
    Review
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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

18 authors at 4 institutions in 1 country.

Xiaomeng ZhangDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.ORCID 0000-0002-3794-6823
Huaning XieDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Pan ChangCentral Laboratory, Second Affiliated Hospital, Xi'an Medical University, Xi'an, Shaanxi, People's Republic of China.
Huishou ZhaoDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Yunlong XiaDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Ling ZhangDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Xiong GuoDepartment of Cardiology, Hospital of People's Liberation Army, Golmud, Qinghai, People's Republic of China.
Chong HuangDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Feng YanDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Lang HuDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Chen LinDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Yueyang LiDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Zhenyu XiongDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Xiong WangDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Guohua LiDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Longxiang DengDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Shan WangDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Ling TaoDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Xijing Hospital · CNGolmud People's Hospital · CNTang Du Hospital · CNXi'an Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Smooth muscle cells (SMCs), which form the walls of blood vessels, play an important role in vascular development and the pathogenic process of vascular remodeling. However, the molecular mechanisms governing SMC differentiation remain poorly understood. Glycoprotein M6B (GPM6B) is a four-transmembrane protein that belongs to the proteolipid protein family and is widely expressed in neurons, oligodendrocytes, and astrocytes. Previous studies have revealed that GPM6B plays a role in neuronal differentiation, myelination, and osteoblast differentiation. In the present study, we found that the GPM6B gene and protein expression levels were significantly upregulated during transforming growth factor-β1 (TGF-β1)-induced SMC differentiation. The knockdown of GPM6B resulted in the downregulation of SMC-specific marker expression and repressed the activation of Smad2/3 signaling. Moreover, GPM6B regulates SMC Differentiation by Controlling TGF-β-Smad2/3 Signaling. Furthermore, we demonstrated that similar to p-Smad2/3, GPM6B was profoundly expressed and coexpressed with SMC differentiation markers in embryonic SMCs. Moreover, GPM6B can regulate the tightness between TβRI, TβRII, or Smad2/3 by directly binding to TβRI to activate Smad2/3 signaling during SMC differentiation, and activation of TGF-β-Smad2/3 signaling also facilitate the expression of GPM6B. Taken together, these findings demonstrate that GPM6B plays a crucial role in SMC differentiation and regulates SMC differentiation through the activation of TGF-β-Smad2/3 signaling via direct interactions with TβRI. This finding indicates that GPM6B is a potential target for deriving SMCs from stem cells in cardiovascular regenerative medicine. Stem Cells 2018 Stem Cells 2019;37:190-201.

Indexed as

AnimalsCell DifferentiationHEK293 CellsHumansMembrane GlycoproteinsMiceMyocytes, Smooth MuscleNerve Tissue ProteinsReceptor, Transforming Growth Factor-beta Type ISignal TransductionSmad2 ProteinSmad3 ProteinTransfectionTransforming Growth Factor beta3Up-RegulationGPM6B protein, humanGpm6b protein, mouseMembrane GlycoproteinsNerve Tissue ProteinsReceptor, Transforming Growth Factor-beta Type ISmad2 ProteinSmad3 ProteinTransforming Growth Factor beta3Cell differentiationGlycoprotein M6BSmooth muscle cellsStem cellsTGF-β pathway

Identifiers

PMID30372567
PMCPMC7379588
OpenAlexW2899233377

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.