Evidence map›Paper›PMID 30385745›Full record

ArticleNature communications2018

Disease-relevant transcriptional signatures identified in individual smooth muscle cells from healthy mouse vessels.

Lina Dobnikar, Annabel L Taylor, Joel Chappell, Phoebe Oldach, Jennifer L Harman, Erin Oerton, Elaine Dzierzak, Martin R Bennett, Mikhail Spivakov, Helle F Jørgensen

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 211 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
211citing papers in PubMed, 2 pooled it
10.3field-weighted citation impact, top 1% 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

211 citing papers in PubMed, 2 syntheses or guidelines pooled it, 304 citations in OpenAlex.

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151 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Lina DobnikarNuclear Dynamics Programme, Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
Annabel L TaylorDivision of Cardiovascular Medicine, University of Cambridge, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK.ORCID http://orcid.org/0000-0003-0319-9716
Joel ChappellDivision of Cardiovascular Medicine, University of Cambridge, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK.
Phoebe OldachNuclear Dynamics Programme, Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
Jennifer L HarmanDivision of Cardiovascular Medicine, University of Cambridge, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK.
Erin OertonNuclear Dynamics Programme, Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.ORCID http://orcid.org/0000-0002-7367-4263
Elaine DzierzakMRC Centre for Inflammation Research, University of Edinburgh, Little France Crescent, Edinburgh, EH16 4TJ, UK.
Martin R BennettDivision of Cardiovascular Medicine, University of Cambridge, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK.
Mikhail SpivakovNuclear Dynamics Programme, Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK. mikhail.spivakov@lms.mrc.ac.uk.ORCID http://orcid.org/0000-0002-0383-3943
Helle F JørgensenDivision of Cardiovascular Medicine, University of Cambridge, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK. hfj22@cam.ac.uk.ORCID http://orcid.org/0000-0002-7909-2977
University of Cambridge · GBBabraham Institute · GBCentre for Inflammation Research · GB

Funding

MOLECULAR BIOLOGY/INTRINSIC PATHWAY FACTOR X ACTIVATIONK08HL001538 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI LOLLAR, JOHN S. · 1985 to 1986
–
British Heart Foundation FS/14/59/31282British Heart Foundation FS/15/38/31516British Heart Foundation PG/12/86/29930British Heart Foundation PG/16/11/32021British Heart Foundation PG/16/63/32307British Heart Foundation RE/13/6/30180British Heart Foundation RG/13/14/30314British Heart Foundation RM/13/3/30159British Heart Foundation (BHF) FS/14/59/31282British Heart Foundation (BHF) FS/15/38/31516British Heart Foundation (BHF) RE/13/6/30180British Heart Foundation (BHF) RM/13/3/30159EC | European Research Council (ERC) AdG 341096Medical Research Council MC_UP_1605/3Medical Research Council (MRC) Core fundingWellcome Trust
6 · The paper itself

Abstract

Vascular smooth muscle cells (VSMCs) show pronounced heterogeneity across and within vascular beds, with direct implications for their function in injury response and atherosclerosis. Here we combine single-cell transcriptomics with lineage tracing to examine VSMC heterogeneity in healthy mouse vessels. The transcriptional profiles of single VSMCs consistently reflect their region-specific developmental history and show heterogeneous expression of vascular disease-associated genes involved in inflammation, adhesion and migration. We detect a rare population of VSMC-lineage cells that express the multipotent progenitor marker Sca1, progressively downregulate contractile VSMC genes and upregulate genes associated with VSMC response to inflammation and growth factors. We find that Sca1 upregulation is a hallmark of VSMCs undergoing phenotypic switching in vitro and in vivo, and reveal an equivalent population of Sca1-positive VSMC-lineage cells in atherosclerotic plaques. Together, our analyses identify disease-relevant transcriptional signatures in VSMC-lineage cells in healthy blood vessels, with implications for disease susceptibility, diagnosis and prevention.

Indexed as

TranscriptomeAnimalsAortaAtaxin-1Carotid ArteriesCell LineageDisease SusceptibilityGene Expression ProfilingMiceMuscle, Smooth, VascularMyocytes, Smooth MusclePlaque, AtheroscleroticSequence Analysis, RNASingle-Cell AnalysisAtaxin-1Atxn1 protein, mouse

Identifiers

PMID30385745
PMCPMC6212435
OpenAlexW2898549090

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.