Evidence map›Paper›PMID 31711674›Full record

ArticleImmunobiology2020

CD163 overexpression using a macrophage-directed gene therapy approach improves wound healing in ex vivo and in vivo human skin models.

David Wilson Ferreira, Cristina Ulecia-Morón, Perla Abigail Alvarado-Vázquez, Katharine Cunnane, Carolina Moracho-Vilriales, Rachel L Grosick, Thiago Mattar Cunha, E Alfonso Romero-Sandoval

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

Article in Immunobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  17. Macrophages in Healing Wounds: Paradoxes and Paradigms.International journal of molecular sciences · 2021
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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 6 institutions in 4 countries.

David Wilson FerreiraDepartment of Pharmacology, University of São Paulo, Ribeirao Preto Medical School, 3900 Bandeirantes Ave., Ribeirão Preto, SP, 14049-900, Brazil; Department of Neurobiology, University of Pittsburgh School of Medicine, 3501 Fifth Ave - BST3, 6th floor, Pittsburgh, PA, 15260, USA. Electronic address: davidferreira_2005@hotmail.com.
Cristina Ulecia-MorónCenter for Biomedical Research Network on Mental Health (CIBERSAM), Avenida Monforte de Lemos, 3-5. Pabellón 11. Planta 0, 28029, Madrid, Spain; Department of Pharmacology and Toxicology, School of Medicine, and Instituto Universitario de Investigación en Neuroquímica (IUIN), Complutense University of Madrid, Avenida Complutense s/n., 28040, Madrid, Spain. Electronic address: cristinaulecia@gmail.com.
Perla Abigail Alvarado-VázquezDepartment of Anesthesiology, Wake Forest School of Medicine, 1 Medical Center Blvd, Winston-Salem, NC, 27157, USA; Department of Medical Biochemistry and Microbiology, BMC, Uppsala University, Husargatan 3, Uppsala, 75123, Sweden. Electronic address: abigail1049@gmail.com.
Katharine CunnaneDepartment of Anesthesiology, Wake Forest School of Medicine, 1 Medical Center Blvd, Winston-Salem, NC, 27157, USA. Electronic address: cunnka16@wfu.edu.
Carolina Moracho-VilrialesDepartment of Pharmaceutical and Administrative Sciences, Presbyterian College School of Pharmacy, 307 N Broad St., Clinton, SC, 29325, USA. Electronic address: carolinamoracho.3@gmail.com.
Rachel L GrosickDepartment of Pharmaceutical and Administrative Sciences, Presbyterian College School of Pharmacy, 307 N Broad St., Clinton, SC, 29325, USA. Electronic address: rlgrosick@presby.edu.
Thiago Mattar CunhaDepartment of Pharmacology, University of São Paulo, Ribeirao Preto Medical School, 3900 Bandeirantes Ave., Ribeirão Preto, SP, 14049-900, Brazil. Electronic address: thicunha@usp.br.
E Alfonso Romero-SandovalDepartment of Anesthesiology, Wake Forest School of Medicine, 1 Medical Center Blvd, Winston-Salem, NC, 27157, USA. Electronic address: earomero.sandoval@gmail.com.
Presbyterian College · USWake Forest University · USCentre for Biomedical Network Research on Rare Diseases · ESUniversidade de São Paulo · BRUniversity of Pittsburgh · USUppsala University · SE

Funding

Training in Mechanisms and Clinical Presentation of PainT32NS073548 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jami Lynn Saloman, BRADLEY K. TAYLOR · 2012 to 2026
$3.1M
Cell-directed therapy using nanotechnology for the prevention of chronic postoperR15GM109333 · NIGMS · PRESBYTERIAN COLLEGE · PI MESSERSMITH, AMY · 2014 to 2014
$331k
NIGMS NIH HHS R15 GM109333NINDS NIH HHS T32 NS073548
6 · The paper itself

Abstract

Large tissue damage or wounds cause serious comorbidities and represent a major burden for patients, families, and health systems. Due to the pivotal role of immune cells in the proper resolution of inflammation and tissue repair, we focus our current study on the interaction of macrophages with skin cells, and specifically on the effects of CD163 gene induction in macrophages in wound healing. We hypothesize that the over-expression of the scavenger receptor gene CD163 in human macrophages would result in a more efficient wound healing process. Using 3D human wounded skin organotypic tissues, we observed that CD163 overexpression in THP-1 and human primary macrophages induced a more efficient re-epithelization when compared to control cells. Using human primary skin cells and an in vitro scratch assay we observed that CD163 overexpression in THP-1 macrophages promoted a more rapid and efficient wound healing process through a unique interaction with fibroblasts. The addition of CD163-blocking antibody, but not isotype control, blocked the efficient wound healing process induced by CD163 overexpression in macrophages. We found that the co-culture of skin cells and CD163 overexpressing macrophages reduced monocyte chemoattractant protein (MCP)-1 and enhanced tumor growth factor (TGF)-α, without altering interleukin (IL)-6 or TGF-β. Our findings show that CD163 induces a more efficient wound healing and seems to promote a wound milieu with a pro-resolution molecular profile. Our studies set the foundation to study this approach in in vivo clinically relevant settings to test its effects in wound healing processes such as acute major injuries, large surgeries, or chronic ulcers.

Indexed as

Antibodies, BlockingAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenChemokine CCL2FibroblastsGenetic TherapyHumansInflammationInterleukin-6KeratinocytesMacrophagesOrgan Culture TechniquesReceptors, Cell SurfaceSkinTHP-1 CellsAntibodies, BlockingAntigens, CDAntigens, Differentiation, MyelomonocyticCCL2 protein, humanCD163 AntigenChemokine CCL2Interleukin-6Receptors, Cell SurfaceTumor Necrosis Factor-alphaFibroblastsGene inductionInflammationKeratinocytesNanoparticleNanotechnologyPostsurgical pain

Identifiers

PMID31711674
PMCPMC7864009
OpenAlexW2983656566

What OpenQuestion holds

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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.