Evidence map›Paper›PMID 24589361›Full record

ArticleBiomaterials2014

The role of macrophage phenotype in vascularization of tissue engineering scaffolds.

Kara L Spiller, Rachel R Anfang, Krista J Spiller, Johnathan Ng, Kenneth R Nakazawa, Jeffrey W Daulton, Gordana Vunjak-Novakovic

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomaterials, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 462 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
462citing papers in PubMed, 1 pooled it
54.3field-weighted citation impact, top 1% 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

462 citing papers in PubMed, 1 synthesis or guideline pooled it, 919 citations in OpenAlex.

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402 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Kara L SpillerDepartment of Biomedical Engineering, Columbia University, 622 West 168th Street, New York, NY 10032, USA; School of Biomedical Engineering, Science, and Health Systems, Drexel University, 3141 Chestnut St., Philadelphia, PA 19104, USA.
Rachel R AnfangDepartment of Biomedical Engineering, Columbia University, 622 West 168th Street, New York, NY 10032, USA.
Krista J SpillerDepartment of Pathology, Columbia University, 630 West 168th Street, New York, NY 10032, USA.
Johnathan NgDepartment of Biomedical Engineering, Columbia University, 622 West 168th Street, New York, NY 10032, USA.
Kenneth R NakazawaDepartment of Biomedical Engineering, Columbia University, 622 West 168th Street, New York, NY 10032, USA.
Jeffrey W DaultonLincoln Laboratory, Massachusetts Institute of Technology, 244 Wood Street, Lexington, MA 02420, USA.
Gordana Vunjak-NovakovicDepartment of Biomedical Engineering, Columbia University, 622 West 168th Street, New York, NY 10032, USA. Electronic address: gv2131@columbia.edu.
Columbia University · USMIT Lincoln Laboratory · US

Funding

Translational Bioreactors - Engineering Complex TissuesP41EB002520 · NIBIB · TUFTS UNIVERSITY MEDFORD · PI KAPLAN, DAVID L. · 2004 to 2018
$16.7M
Engineering Vascularized Cardiac MuscleR01HL076485 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Gordana Vunjak-Novakovic · 2005 to 2026
$9.2M
Craniofacial Tissue EngineeringR01DE016525 · NIDCR · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI VUNJAK-NOVAKOVIC, GORDANA · 2005 to 2017
$5.5M
NHLBI NIH HHS R01 HL076485NIBIB NIH HHS EB002520NIBIB NIH HHS P41 EB002520NIDCR NIH HHS R01 DE016525
6 · The paper itself

Abstract

Angiogenesis is crucial for the success of most tissue engineering strategies. The natural inflammatory response is a major regulator of vascularization, through the activity of different types of macrophages and the cytokines they secrete. Macrophages exist on a spectrum of diverse phenotypes, from "classically activated" M1 to "alternatively activated" M2 macrophages. M2 macrophages, including the subsets M2a and M2c, are typically considered to promote angiogenesis and tissue regeneration, while M1 macrophages are considered to be anti-angiogenic, although these classifications are controversial. Here we show that in contrast to this traditional paradigm, primary human M1 macrophages secrete the highest levels of potent angiogenic stimulators including VEGF; M2a macrophages secrete the highest levels of PDGF-BB, a chemoattractant for stabilizing pericytes, and also promote anastomosis of sprouting endothelial cells in vitro; and M2c macrophages secrete the highest levels of MMP9, an important protease involved in vascular remodeling. In a murine subcutaneous implantation model, porous collagen scaffolds were surrounded by a fibrous capsule, coincident with high expression of M2 macrophage markers, while scaffolds coated with the bacterial lipopolysaccharide were degraded by inflammatory macrophages, and glutaraldehyde-crosslinked scaffolds were infiltrated by substantial numbers of blood vessels, accompanied by high levels of M1 and M2 macrophages. These results suggest that coordinated efforts by both M1 and M2 macrophages are required for angiogenesis and scaffold vascularization, which may explain some of the controversy over which phenotype is the angiogenic phenotype.

Indexed as

Neovascularization, PhysiologicAnimalsBecaplerminCells, CulturedHumansHuman Umbilical Vein Endothelial CellsMacrophagesMaleMiceMice, Inbred C57BLProto-Oncogene Proteins c-sisTissue EngineeringTissue ScaffoldsVascular Endothelial Growth Factor ABecaplerminProto-Oncogene Proteins c-sisVascular Endothelial Growth Factor AAngiogenesisCollagenForeign body responseInflammationMacrophage

Identifiers

PMID24589361
PMCPMC4000280
OpenAlexW2085701716

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.