Evidence map›Paper›PMID 23129751›Full record

ArticleThe Journal of experimental medicine2012

Procontractile G protein-mediated signaling pathways antagonistically regulate smooth muscle differentiation in vascular remodeling.

Till F Althoff, Julián Albarrán Juárez, Kerstin Troidl, Cong Tang, Shengpeng Wang, Angela Wirth, Mikito Takefuji, Nina Wettschureck, Stefan Offermanns

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  6. Ca2+/calmodulin-dependent protein kinase II-γ (CaMKIIγ) negatively regulates vascular smooth muscle cell proliferation and vascular remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  7. Review
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  9. Lysophospholipid mediators in the vasculature.Experimental cell research · 2015
    Review
  10. Article
  11. Article
  12. 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

9 authors at 3 institutions in 1 country.

Till F AlthoffDepartment of Pharmacology, Max-Planck-Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Julián Albarrán Juárez
Kerstin Troidl
Cong Tang
Shengpeng Wang
Angela Wirth
Mikito Takefuji
Nina Wettschureck
Stefan Offermanns
Max Planck Institute for Heart and Lung Research · DEGoethe University Frankfurt · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular smooth muscle (Sm) cells (VSMCs) are highly plastic. Their differentiation state can be regulated by serum response factor (SRF), which activates genes involved in Sm differentiation and proliferation by recruiting cofactors, such as members of the myocardin family and ternary complex factors (TCFs), respectively. However, the extracellular cues and upstream signaling mechanisms regulating SRF-dependent VSMC differentiation under in vivo conditions are poorly understood. In this study, we show that the procontractile signaling pathways mediated by the G proteins G(12)/G(13) and G(q)/G(11) antagonistically regulate VSMC plasticity in different models of vascular remodeling. In mice lacking Gα(12)/Gα(13) or their effector, the RhoGEF protein LARG, RhoA-dependent SRF-regulation was blocked and down-regulation of VSMC differentiation marker genes was enhanced. This was accompanied by an excessive vascular remodeling and exacerbation of atherosclerosis. In contrast, Sm-specific Gα(q)/Gα(11) deficiency blocked activation of extracellular signal-regulated kinase 1/2 and the TCF Elk-1, resulting in a reduced VSMC dedifferentiation in response to flow cessation or vascular injury. These data show that the balanced activity of both G protein-mediated pathways in VSMCs is required for an appropriate vessel remodeling response in vascular diseases and suggest new approaches to modulate Sm differentiation in vascular pathologies.

Indexed as

AnimalsApolipoproteins EBlood PressureBlotting, WesternCell DifferentiationDNA PrimersEnzyme ActivationGene Expression RegulationGTP-Binding ProteinsGuanine Nucleotide Exchange FactorsImmunohistochemistryMaleMiceMice, KnockoutMuscle, Smooth, VascularReal-Time Polymerase Chain ReactionApolipoproteins EArhgef12 protein, mouseDNA PrimersGTP-Binding ProteinsGuanine Nucleotide Exchange FactorsRho Guanine Nucleotide Exchange FactorsSerum Response Factor

Identifiers

PMID23129751
PMCPMC3501360
OpenAlexW2136589598

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.