Evidence map›Paper›PMID 25309723›Full record

ArticleVascular cell2014

Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury.

Brian Paul Herring, April M Hoggatt, Christopher Burlak, Stefan Offermanns

Open access · diamondAbstract read
In one paragraph

Article in Vascular cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

106 citing papers in PubMed, 142 citations in OpenAlex.

  1. Mesenchymal R-spondin 3 promotes an immunogenic tumor microenvironment with adaptive immune resistance in human gastric adenocarcinoma.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026
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46 more citing papers are in PubMed but not listed here.

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

4 authors at 4 institutions in 2 countries.

Brian Paul HerringDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
April M HoggattDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Christopher BurlakDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA ; Department of Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA ; Current address: Schultz Diabetes Institute, Department of Surgery, University of Minnesota, Minneapolis, MN 55455, USA.
Stefan OffermannsDepartment of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Ludwigstr. 43, 61231 Bad Nauheim, Germany.
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineMax Planck Institute for Heart and Lung Research · DEUniversity of Minnesota · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation.

methodsWe utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive cells to the neointima determined.

resultsAnalysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive cells derived from either Mhy11 or Acta2 tagged medial vascular smooth muscle cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively).

conclusionThese data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth muscle cells.

Indexed as

NeointimaSmooth muscle myosinSmooth muscle α-actinVascular smooth muscle

Identifiers

PMID25309723
PMCPMC4193961
OpenAlexW2048656545

What OpenQuestion holds

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LicenceCC BY
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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.