Evidence map›Paper›PMID 41121373›Full record

ArticleStem cell research & therapy2025

Mesenchymal stromal cells modulate neutrophil phenotype via paracrine signals.

Laudy Cherry, Sinziana Popescu, Carmen Alexandra Neculachi, Evelyn-Gabriela Nastase-Rusu, Catalina Iolanda Marinescu-Colan, Bogdan Paul Cosman, Letitia Ciortan, Fabio Martelli, Maya Simionescu, Elena Butoi and 2 more

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
4 · The record

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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

12 authors.

Laudy Cherry *Institute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Sinziana Popescu *Institute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Carmen Alexandra NeculachiInstitute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Evelyn-Gabriela Nastase-RusuInstitute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Catalina Iolanda Marinescu-ColanInstitute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Bogdan Paul CosmanInstitute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Letitia CiortanInstitute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Fabio MartelliInstitute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Maya SimionescuInstitute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Elena ButoiInstitute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Alexandrina BurlacuInstitute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania.
Mihai Bogdan PredaInstitute of Cellular Biology and Pathology "Nicolae Simionescu", Romanian Academy, 050568, Bucharest, Romania. bogdan.preda@icbp.ro.

Funding

Ministero della Salute POS-T4 CAL.HUB.RIA T4-AN-09Ministerul Cercetării şi Inovării PN-III-P4-ID-PCCF-2016-0172, contract no 5/01.07.2018NextGenerationEU contract no. 760062/23.05.2034, application no. 186/24.11.2022
6 · The paper itself

Abstract

backgroundDespite the recognized importance of neutrophils in cardiac repair following myocardial infarction (MI), their interaction with mesenchymal stromal cells (MSCs), particularly regarding polarization phenotypes and functional impacts, remains unclear. Here, we investigated these interactions across controlled in vitro systems and an in vivo MI model.

methodsHuman HL-60 cells were differentiated into neutrophil-like cells (dHL-60) and polarized toward N1/N2 states to test the MSC paracrine effects using indirect transwell coculture. Readouts included gene expression, cytokine profiling and functional assays. To increase translational relevance, indirect ex vivo cocultures of human MSCs with primary neutrophils isolated from MI mice or from MI patients were analysed for gene expression and cytokine profiles in conditioned media. In vivo, syngeneic mouse MSCs were transplanted subcutaneously immediately after MI, and early cardiac function was evaluated by echocardiography. Cardiac neutrophils where quantified by flow cytometry, and Ly6G

resultsIn vitro, MSCs suppressed pro-inflammatory mediators in N1-like neutrophils and enhanced reparative factors in N2-like cells. In vivo, remote MSC transplantation improved early cardiac performance, and reduced neutrophil accumulation in the infarct. Paradoxically, cardiac neutrophils showed transcriptomic enrichment of inflammatory pathways, whereas blood neutrophils showed reduced interferon-related programs.

conclusionOur findings indicate that MSCs can modulate neutrophil responses, underscoring the nuanced effects of MSC-based approaches in ischemic heart disease. These results suggest that anti-inflammatory effects observed under controlled conditions may not fully translate in vivo, highlighting the importance of context when evaluating MSC-based therapies.

Indexed as

Mesenchymal Stem CellsMyocardial InfarctionNeutrophilsParacrine CommunicationAnimalsCell DifferentiationCoculture TechniquesHL-60 CellsHumansMaleMesenchymal Stem Cell TransplantationMicePhenotypeInflammationMesenchymal stromal cellsMyocardial infarctionNeutrophilsRemote cell therapy

Identifiers

PMID41121373
PMCPMC12539047

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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.