Evidence map›Paper›PMID 28348370›Full record

ArticleScientific reports2017

Non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury.

Claire E Olingy, Cheryl L San Emeterio, Molly E Ogle, Jack R Krieger, Anthony C Bruce, David D Pfau, Brett T Jordan, Shayn M Peirce, Edward A Botchwey

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

135 citing papers in PubMed, 223 citations in OpenAlex.

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  16. Impaired CAMK4 Activity Limits Atherosclerosis and Reprograms Myelopoiesis.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
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  20. Resolvin D2 restores monocyte anisocytosis and mediates a shift toward classical monocytes ex vivo in blood samples from patients after major burns.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article

75 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 1 country.

Claire E OlingyWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 315 Ferst Drive, Atlanta, GA, 30332, USA.ORCID 0000-0002-4449-4319
Cheryl L San EmeterioWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 315 Ferst Drive, Atlanta, GA, 30332, USA.
Molly E OgleWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 315 Ferst Drive, Atlanta, GA, 30332, USA.
Jack R KriegerWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 315 Ferst Drive, Atlanta, GA, 30332, USA.
Anthony C BruceDepartment of Biomedical Engineering, University of Virginia, Box 800759, Charlottesville, VA, 22908, USA.
David D PfauWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 315 Ferst Drive, Atlanta, GA, 30332, USA.
Brett T JordanWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 315 Ferst Drive, Atlanta, GA, 30332, USA.
Shayn M PeirceWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 315 Ferst Drive, Atlanta, GA, 30332, USA.
Edward A BotchweyWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 315 Ferst Drive, Atlanta, GA, 30332, USA. edward.botchwey@bme.gatech.edu.ORCID 0000-0003-1140-5786
Georgia Institute of Technology · USUniversity of Virginia · US

Funding

Phospholipid Growth Factors for Therapeutic Arteriogenesis and Tissue EngineeringR01AR056445 · NIAMS · UNIVERSITY OF VIRGINIA · PI BOTCHWEY, EDWARD A. · 2009 to 2014
$1.8M
Therapeutic S1P Drug Targets for Cranial Bone RepairR01DE019935 · NIDCR · UNIVERSITY OF VIRGINIA · PI BOTCHWEY, EDWARD A. · 2009 to 2013
$1.8M
NIAMS NIH HHS R01 AR056445NIDCR NIH HHS R01 DE019935
6 · The paper itself

Abstract

Successful tissue repair requires the activities of myeloid cells such as monocytes and macrophages that guide the progression of inflammation and healing outcome. Immunoregenerative materials leverage the function of endogenous immune cells to orchestrate complex mechanisms of repair; however, a deeper understanding of innate immune cell function in inflamed tissues and their subsequent interactions with implanted materials is necessary to guide the design of these materials. Blood monocytes exist in two primary subpopulations, characterized as classical inflammatory or non-classical. While classical monocytes extravasate into inflamed tissue and give rise to macrophages or dendritic cells, the recruitment kinetics and functional role of non-classical monocytes remains unclear. Here, we demonstrate that circulating non-classical monocytes are directly recruited to polymer films within skin injuries, where they home to a perivascular niche and generate alternatively activated, wound healing macrophages. Selective labeling of blood monocyte subsets indicates that non-classical monocytes are biased progenitors of alternatively activated macrophages. On-site delivery of the immunomodulatory small molecule FTY720 recruits S1PR3-expressing non-classical monocytes that support vascular remodeling after injury. These results elucidate a previously unknown role for blood-derived non-classical monocytes as contributors to alternatively activated macrophages, highlighting them as key regulators of inflammatory response and regenerative outcome.

Indexed as

Wound HealingAdoptive TransferAnimalsAntigens, CDArteriolesBiocompatible MaterialsCell DifferentiationFingolimod HydrochlorideImplants, ExperimentalMacrophage ActivationMacrophagesMaleMice, Inbred C57BLModels, BiologicalMonocytesSkinAntigens, CDBiocompatible MaterialsFingolimod Hydrochloride

Identifiers

PMID28348370
PMCPMC5428475
OpenAlexW2599257356

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.