Evidence map›Paper›PMID 25765938›Full record

ArticleCardiovascular research2015

Chemokine receptors CXCR2 and CX3CR1 differentially regulate functional responses of bone-marrow endothelial progenitors during atherosclerotic plaque regression.

Oana Herlea-Pana, Longbiao Yao, Janet Heuser-Baker, Qiongxin Wang, Qilong Wang, Constantin Georgescu, Ming-Hui Zou, Jana Barlic-Dicen

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 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

8 authors at 2 institutions in 1 country.

Oana Herlea-PanaCardiovascular Biology, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USA.
Longbiao YaoCardiovascular Biology, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USA.
Janet Heuser-BakerCardiovascular Biology, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USA.
Qiongxin WangDivision of Molecular Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Qilong WangDivision of Molecular Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Constantin GeorgescuArthritis and Clinical Immunology Programs, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
Ming-Hui ZouDivision of Molecular Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Jana Barlic-DicenCardiovascular Biology, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USA jana-barlic-dicen@omrf.org.
Oklahoma Medical Research Foundation · USUniversity of Oklahoma Health Sciences Center · US

Funding

SWI/SNF-REGULATED POSTNATAL ANGIOGENESISP20RR018758 · NCRR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI XIA, LIJUN · 2003 to 2011
$14.9M
Interdisciplinary research in vascular biologyP20GM103441 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MCEVER, RODGER PAUL · 2012 to 2014
$7.3M
NCRR NIH HHS 5 P20 RR018758-08NIGMS NIH HHS 8 P20 GM103441-08
6 · The paper itself

Abstract

aimsAtherosclerosis manifests itself as arterial plaques, which lead to heart attacks or stroke. Treatments supporting plaque regression are therefore aggressively pursued. Studies conducted in models in which hypercholesterolaemia is reversible, such as the Reversa mouse model we have employed in the current studies, will be instrumental for the development of such interventions. Using this model, we have shown that advanced atherosclerosis regression occurs when lipid lowering is used in combination with bone-marrow endothelial progenitor cell (EPC) treatment. However, it remains unclear how EPCs home to regressing plaques and how they augment atherosclerosis reversal. Here we identify molecules that support functional responses of EPCs during plaque resolution. METHODS AND

resultsChemokines CXCL1 and CX3CL1 were detected in the vascular wall of atheroregressing Reversa mice, and their cognate receptors CXCR2 and CX3CR1 were observed on adoptively transferred EPCs in circulation. We tested whether CXCL1-CXCR2 and CX3CL1-CX3CR1 axes regulate functional responses of EPCs during plaque reversal. We show that pharmacological inhibition of CXCR2 or CX3CR1, or genetic inactivation of these two chemokine receptors interfered with EPC-mediated advanced atherosclerosis regression. We also demonstrate that CXCR2 directs EPCs to regressing plaques while CX3CR1 controls a paracrine function(s) of these cells.

conclusionCXCR2 and CX3CR1 differentially regulate EPC functional responses during atheroregression. Our study improves understanding of how chemokines and chemokine receptors regulate plaque resolution, which could determine the effectiveness of interventions reducing complications of atherosclerosis.

Indexed as

AnimalsBone MarrowCells, CulturedCX3C Chemokine Receptor 1Disease Models, AnimalEndothelial CellsMice, Inbred C57BLMice, TransgenicPlaque, AtheroscleroticReceptors, ChemokineReceptors, Interleukin-8BCX3C Chemokine Receptor 1Cx3cr1 protein, mouseReceptors, ChemokineReceptors, Interleukin-8BAtherosclerosis regressionChemokine receptor CX3CR1Chemokine receptor CXCR2Endothelial progenitor cell

Identifiers

PMID25765938
PMCPMC4481573
OpenAlexW2130361132

What OpenQuestion holds

Textmetadata
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.