Evidence map›Paper›PMID 32494664›Full record

ArticleScience advances2020

Macrophages of diverse phenotypes drive vascularization of engineered tissues.

P L Graney, S Ben-Shaul, S Landau, A Bajpai, B Singh, J Eager, A Cohen, S Levenberg, K L Spiller

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 1 pooled it
12.6field-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

136 citing papers in PubMed, 1 synthesis or guideline pooled it, 276 citations in OpenAlex.

  1. Modeling Immunity In Vitro: Slices, Chips, and Engineered Tissues.Annual review of biomedical engineering · 2021
    Pooled it
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  19. M2c Macrophages Mediate YAP1 to Promote Vascularized Bone Regeneration in Distraction Osteogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  20. Affinity-based controlled release of interleukin-4 from scaffolds via biotin-streptavidin interactions for immunomodulation.Journal of controlled release : official journal of the Controlled Release Society · 2025
    Article

76 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

9 authors at 2 institutions in 2 countries.

P L GraneySchool of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA, USA.ORCID 0000-0003-0428-2634
S Ben-ShaulDepartment of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.ORCID 0000-0002-0719-4392
S LandauDepartment of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.ORCID 0000-0002-3514-3656
A BajpaiSchool of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA, USA.
B SinghSchool of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA, USA.ORCID 0000-0001-6915-6618
J EagerSchool of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA, USA.ORCID 0000-0002-0344-4323
A CohenDepartment of Electrical and Computer Engineering, Drexel University, Philadelphia, PA, USA.ORCID 0000-0002-7707-5970
S LevenbergDepartment of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.ORCID 0000-0001-5471-7339
K L SpillerSchool of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA, USA.ORCID 0000-0001-7798-1490
Drexel University · USTechnion – Israel Institute of Technology · IL

Funding

Understanding and Controlling Macrophage Behavior in AngiogenesisR01HL130037 · NHLBI · DREXEL UNIVERSITY · PI SPILLER, KARA LORRAINE · 2016 to 2024
$4.7M
NHLBI NIH HHS R01 HL130037
6 · The paper itself

Abstract

Macrophages are key contributors to vascularization, but the mechanisms behind their actions are not understood. Here, we show that diverse macrophage phenotypes have distinct effects on endothelial cell behavior, with resulting effects on vascularization of engineered tissues. In Transwell coculture, proinflammatory M1 macrophages caused endothelial cells to up-regulate genes associated with sprouting angiogenesis, whereas prohealing (M2a), proremodeling (M2c), and anti-inflammatory (M2f) macrophages promoted up-regulation of genes associated with pericyte cell differentiation. In 3D tissue-engineered human blood vessel networks in vitro, short-term exposure (1 day) to M1 macrophages increased vessel formation, while long-term exposure (3 days) caused regression. When human tissue-engineered blood vessel networks were implanted into athymic mice, macrophages expressing markers of both M1 and M2 phenotypes wrapped around and bridged adjacent vessels and formed vessel-like structures themselves. Last, depletion of host macrophages inhibited remodeling of engineered vessels, infiltration of host vessels, and anastomosis with host vessels.

Indexed as

Endothelial CellsTissue EngineeringAnimalsCell DifferentiationMacrophagesMicePhenotype

Identifiers

PMID32494664
PMCPMC7195167
OpenAlexW3021656578

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.