Evidence map›Paper›PMID 19734197›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2009

Bone marrow-derived cell-specific chemokine (C-C motif) receptor-2 expression is required for arteriolar remodeling.

Meghan M Nickerson, Ji Song, Joshua K Meisner, Sameer Bajikar, Caitlin W Burke, Casey W Shuptrine, Gary K Owens, Thomas C Skalak, Richard J Price

Abstract readComparative Study
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. MicroRNA-146a Regulates Perfusion Recovery in Response to Arterial OcclusionFrontiers in bioengineering and biotechnology · 2018
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  9. Macrophages in collateral arteriogenesis.Frontiers in physiology · 2012
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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

9 authors at 1 institution in 1 country.

Meghan M NickersonDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA.
Ji Song
Joshua K Meisner
Sameer Bajikar
Caitlin W Burke
Casey W Shuptrine
Gary K Owens
Thomas C Skalak
Richard J Price
University of Virginia · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007267 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GARCIA-BLANCO, MARIANO A. · 1985 to 2024
$13.4M
Integrated Control of Vascular Pattern FormationR01HL065958 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI SKALAK, THOMAS C · 2001 to 2005
$3.5M
Arteriogenesis by Ultrasonic Microbubble DestructionR01HL074082 · NHLBI · UNIVERSITY OF VIRGINIA · PI PRICE, RICHARD J. · 2006 to 2010
$1.7M
NHLBI NIH HHS HL065958NHLBI NIH HHS HL074082NHLBI NIH HHS R01 HL065958NHLBI NIH HHS R01 HL074082
6 · The paper itself

Abstract

objectiveBone marrow-derived cells (BMCs) and inflammatory chemokine receptors regulate arteriogenesis and angiogenesis. Here, we tested whether arteriolar remodeling in response to an inflammatory stimulus is dependent on BMC-specific chemokine (C-C motif) receptor 2 (CCR2) expression and whether this response involves BMC transdifferentiation into smooth muscle. METHODS AND

resultsDorsal skinfold window chambers were implanted into C57Bl/6 wild-type (WT) mice, as well as the following bone marrow chimeras (donor-host): WT-WT, CCR2(-/-)-WT, WT-CCR2(-/-), and EGFP(+)-WT. One day after implantation, tissue MCP-1 levels rose from "undetectable" to 463 pg/mg, and the number of EGFP(+) cells increased more than 4-fold, indicating marked inflammation. A 66% (28 microm) increase in maximum arteriolar diameter was observed over 7 days in WT-WT mice. This arteriolar remodeling response was completely abolished in CCR2(-/-)-WT mice but largely rescued in WT-CCR2(-/-) mice. EGFP(+) BMCs were numerous throughout the tissue, but we found no evidence that EGFP(+) BMCs transdifferentiate into smooth muscle, based on examination of >800 arterioles and venules.

conclusionsBMC-specific CCR2 expression is required for injury/inflammation-associated arteriolar remodeling, but this response is not characterized by the differentiation of BMCs into smooth muscle.

Indexed as

Analysis of VarianceAnimalsArteriolesBone Marrow CellsBone Marrow TransplantationCell ProliferationCells, CulturedDisease Models, AnimalGene Expression RegulationMiceMice, Inbred C57BLMice, KnockoutMyocytes, Smooth MuscleNeovascularization, PhysiologicProbabilityRandom AllocationReceptors, CCR2

Identifiers

PMID19734197
PMCPMC2766019
OpenAlexW2129105801

What OpenQuestion holds

Textmetadata
LicenceTDM
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.