Evidence map›Paper›PMID 36278486›Full record

ArticleJCI insight2022

Distinct patterns of responses in endothelial cells and smooth muscle cells following vascular injury.

Xili Ding, Qin An, Weikang Zhao, Yang Song, Xiaokai Tang, Jing Wang, Chih-Chiang Chang, Gexin Zhao, Tzung Hsiai, Guoping Fan and 2 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. 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
0.8field-weighted citation impact, top 29% 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, 12 citations in OpenAlex.

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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

12 authors at 2 institutions in 2 countries.

Xili DingDepartment of Bioengineering, University of California, Los Angeles, California, USA.
Qin AnDepartment of Human Genetics, David Geffen School of Medicine.
Weikang ZhaoDepartment of Bioengineering, University of California, Los Angeles, California, USA.
Yang SongDepartment of Bioengineering, University of California, Los Angeles, California, USA.
Xiaokai TangKey Laboratory for Biomechanics and Mechanobiology of Ministry of Education, Beijing Advanced Innovation Center for Biomedical Engineering, School of Biological Science and Medical Engineering, Beihang University, Beijing, China.
Jing WangDepartment of Human Genetics, David Geffen School of Medicine.
Chih-Chiang ChangDepartment of Bioengineering, University of California, Los Angeles, California, USA.
Gexin ZhaoDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, and.
Tzung HsiaiDepartment of Bioengineering, University of California, Los Angeles, California, USA.
Guoping FanDepartment of Human Genetics, David Geffen School of Medicine.
Yubo FanSchool of Engineering Medicine and.
Song LiDepartment of Bioengineering, University of California, Los Angeles, California, USA.
University of California, Los Angeles · USBeihang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular smooth muscle cells (SMCs) are heterogeneous, and their differential responses to vascular injury are not well understood. To address this question, we performed single-cell analysis of vascular cells to a ligation injury in mouse carotid arteries after 3 days. While endothelial cells had a homogeneous activation of mesenchymal genes, less than 30% of SMCs responded to the injury and generated 2 distinct clusters - i.e., proinflammatory SMCs and stress-responsive SMCs. Proinflammatory SMCs were enriched with high levels of inflammatory markers such as vascular cell adhesion molecule-1 while stress-responsive SMCs overexpressed heat shock proteins. Trajectory analysis suggested that proinflammatory SMCs were potentially derived from a specific subpopulation of SMCs. Ligand-receptor pair analysis showed that the interaction between macrophages and proinflammatory SMCs was the major cell-cell communication among all cell types in the injured arteries. In vitro coculture demonstrated that VCAM1+ SMCs had a stronger chemotactic effect on macrophage recruitment than VCAM1- SMCs. Consistently, the number of VCAM1+ SMCs significantly increased in injured arteries and atherosclerotic lesions of ApoE-/- mice and human arteries. These findings provide insights at the single-cell level on the distinct patterns of endothelial cells and SMC responses to vascular injury.

Indexed as

Endothelial CellsVascular System InjuriesAnimalsApolipoproteins EHeat-Shock ProteinsHumansLigandsMiceMice, Knockout, ApoEMuscle, Smooth, VascularMyocytes, Smooth MuscleVascular Cell Adhesion Molecule-1Apolipoproteins EHeat-Shock ProteinsLigandsVascular Cell Adhesion Molecule-1Cardiovascular diseaseVascular Biology

Identifiers

PMID36278486
PMCPMC9714785
OpenAlexW4307106010

What OpenQuestion holds

Textmetadata
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.