Evidence map›Paper›PMID 27148736›Full record

ArticlePloS one2016

Dendritic Cells Expressing Triggering Receptor Expressed on Myeloid Cells-1 Correlate with Plaque Stability in Symptomatic and Asymptomatic Patients with Carotid Stenosis.

Vikrant Rai, Velidi H Rao, Zhifei Shao, Devendra K Agrawal

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

44 citing papers in PubMed, 76 citations in OpenAlex.

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  14. Therapeutic Potential of Targeting p27Archives of internal medicine research · 2024
    Article
  15. Article
  16. Role of oncostatin-M in ECM remodeling and plaque vulnerability.Molecular and cellular biochemistry · 2023
    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

4 authors at 1 institution in 1 country.

Vikrant RaiDepartment of Clinical and Translational Science, Creighton University School of Medicine, Omaha, Nebraska 68178, United States of America.
Velidi H RaoDepartment of Clinical and Translational Science, Creighton University School of Medicine, Omaha, Nebraska 68178, United States of America.
Zhifei ShaoDepartment of Clinical and Translational Science, Creighton University School of Medicine, Omaha, Nebraska 68178, United States of America.
Devendra K AgrawalDepartment of Clinical and Translational Science, Creighton University School of Medicine, Omaha, Nebraska 68178, United States of America.
Creighton University · US

Funding

VITAMIN D AND IMMUNOMODULATION IN CORONARY ARTERY DISEASER01HL116042 · NHLBI · CREIGHTON UNIVERSITY · PI AGRAWAL, DEVENDRA K. · 2012 to 2016
$3.3M
APOPTOSIS OF SMOOTH MUSCLE CELLS IN CAROTID PLAQUESR01HL073349 · NHLBI · CREIGHTON UNIVERSITY · PI AGRAWAL, DEVENDRA K. · 2004 to 2013
$2.6M
NHLBI NIH HHS R01 HL073349NHLBI NIH HHS R01 HL116042
6 · The paper itself

Abstract

Atherosclerosis is a chronic inflammatory disease with atherosclerotic plaques containing inflammatory cells, including T-lymphocytes, dendritic cells (DCs) and macrophages that are responsible for progression and destabilization of atherosclerotic plaques. Stressed cells undergoing necrosis release molecules that act as endogenous danger signals to alert and activate innate immune cells. In atherosclerotic tissue the number of DCs increases with the progression of the lesion and produce several inflammatory cytokines and growth factors. Triggering receptor expressed on myeloid cells (TREM)-1 plays a crucial role in inflammation. However, relationship of DCs and the role of TREM-1 with the stability of atherosclerotic plaques have not been examined. In this study, we investigated the heterogeneity of the plaque DCs, myeloid (mDC1 and mDC2) and plasmacytoid (pDCs), and examined the expression of TREM-1 and their co-localization with DCs in the plaques from symptomatic (S) and asymptomatic (AS) patients with carotid stenosis. We found increased expression of HLA-DR, fascin, and TREM-1 and decreased expression of TREM-2 and α-smooth muscle actin in S compared to AS atherosclerotic carotid plaques. Both TREM-1 and fascin were co-localized suggesting increased expression of TREM-1 in plaque DCs of S compared to AS patients. These data were supported by increased mRNA transcripts of TREM-1 and decreased mRNA transcripts of TREM-2 in carotid plaques of S compared to AS patients. There was higher density of both CD1c+ mDC1 and CD141+ mDC2 in the carotid plaques from AS compared to S patients, where as the density of CD303+ pDCs were higher in the carotid plaques of S compared to AS patients. These findings suggest a potential role of pDCs and TREM-1 in atherosclerotic plaque vulnerability. Thus, newer therapies could be developed to selectively block TREM-1 for stabilizing atherosclerotic plaques.

Indexed as

ActinsCarotid StenosisCase-Control StudiesDendritic CellsEndarterectomy, CarotidFemaleHLA-DR AntigensHumansMaleMembrane GlycoproteinsPlaque, AtheroscleroticReceptors, ImmunologicRNA, MessengerTriggering Receptor Expressed on Myeloid Cells-1ACTA2 protein, humanActinsHLA-DR AntigensMembrane GlycoproteinsReceptors, ImmunologicRNA, MessengerTREM1 protein, humanTREM2 protein, humanTriggering Receptor Expressed on Myeloid Cells-1

Identifiers

PMID27148736
PMCPMC4858252
OpenAlexW2383633934

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.