Evidence map›Paper›PMID 39565311›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

In situ licensing of mesenchymal stem cell immunomodulatory function via BMP-2 induced developmental process.

Fuwei Zhu, Luli Ji, Kai Dai, Shunshu Deng, Jing Wang, Changsheng Liu

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Article
  8. Development-based In Vivo Bioreactor Strategy for Challenging Senescent Bone Reconstruction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  15. Bone organoid construction and evolution.Journal of orthopaedic translation · 2025
    Review
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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

6 authors.

Fuwei ZhuThe State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, People's Republic of China.ORCID 0009-0008-7975-9250
Luli JiThe State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, People's Republic of China.
Kai DaiThe State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, People's Republic of China.ORCID 0000-0002-6551-8463
Shunshu DengThe State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, People's Republic of China.
Jing WangThe State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, People's Republic of China.ORCID 0000-0002-6326-4869
Changsheng LiuSchool of Materials Science and Engineering, Engineering Research Center for Biomedical Materials of the Ministry of Education, East China University of Science and Technology, Shanghai 200237, People's Republic of China.

Funding

Foundation of Frontiers Science the Center for Materiobiology and Dynamic Chemistry JKVD1211002the Basic Science Center Program T2288102the Key Program of the National Natural Science Foundation of China 32230059
6 · The paper itself

Abstract

The immunomodulatory function of mesenchymal stem cells (MSCs) is plastic and susceptible to resident microenvironment in vivo or inflammatory factors in vitro. We propose a unique method to enhance the immunoregulatory functions of mesenchymal stem cells (MSCs) through an artificially controllable in vivo inflammatory microenvironment generated by biomaterials loaded with BMP-2 that induce bone development. MSCs activated through this method effectively induce M1 macrophage polarization toward the M2 phenotype, promote differentiation of naïve T cells into regulatory T cells, and inhibit the proliferation of activated T cells via prostaglandin E2 (PGE2) secretion. This in vivo licensing not only preserves the immunogenicity of MSCs but also alters DNA methylation patterns, enabling MSCs to exhibit immunoregulatory effects with epigenetic memory. Validation in a mouse colitis model demonstrated their therapeutic efficacy and long-term viability. Furthermore, we found that the material composition influences the inflammatory response during development, with polysaccharide-based biomaterials proving advantageous over protein-based materials in establishing an inflammatory niche conducive to MSC activity. These findings underscore the potential of tissue engineering to create in vivo environments that license MSCs, offering a strategic avenue to enhance MSC-based therapies for addressing significant immune disorders.

Indexed as

Bone Morphogenetic Protein 2Cell DifferentiationColitisMesenchymal Stem CellsAnimalsDinoprostoneHumansImmunomodulationMacrophagesMesenchymal Stem Cell TransplantationMiceMice, Inbred C57BLT-Lymphocytes, RegulatoryBone Morphogenetic Protein 2Dinoprostoneimmunogenicityimmunomodulatoryinflammatorymesenchymal stem cellsosteo-organoids

Identifiers

PMID39565311
PMCPMC11621467

What OpenQuestion holds

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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.