Evidence map›Paper›PMID 42482158›Full record

ArticleStem cell research & therapy2026

Neuroprotective effect of mesenchymal stem cell-derived miR-143-3p on dopaminergic neurons via the TLR3/NF-κB/p53 signaling pathway.

Jing Sun, Tian Wang, Chen Qiu, Tianwen Li, Peng Wang, Tatyana Matveeva, Tanner Boyd, Qingyuan Tang, Jun Xue, Lu Su and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Jing Sun *State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science, Institute for Translational Brain Research, Fudan University, Shanghai, 200032, China.
Tian Wang *State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science, Institute for Translational Brain Research, Fudan University, Shanghai, 200032, China.
Chen Qiu *Laboratory for Regenerative Cell Therapy, Department of Neurosurgery, Massachusetts General Hospital, George A. ''Doc'' Lopez, Harvard Medical School, Boston, MA, 02114, USA.
Tianwen LiDepartment of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Peng WangDepartment of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Tatyana MatveevaLaboratory for Regenerative Cell Therapy, Department of Neurosurgery, Massachusetts General Hospital, George A. ''Doc'' Lopez, Harvard Medical School, Boston, MA, 02114, USA.
Tanner BoydLaboratory for Regenerative Cell Therapy, Department of Neurosurgery, Massachusetts General Hospital, George A. ''Doc'' Lopez, Harvard Medical School, Boston, MA, 02114, USA.
Qingyuan TangLaboratory for Regenerative Cell Therapy, Department of Neurosurgery, Massachusetts General Hospital, George A. ''Doc'' Lopez, Harvard Medical School, Boston, MA, 02114, USA.
Jun XueDepartment of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Lu SuState Key Laboratory of Brain Function and Disorders, Department of Neurology and National Research Center for Aging and Medicine, National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Hyemyung SeoDepartment of Molecular Medicine, School of Bio-Pharmaceutical Convergence, Institute for Precision Therapeutics, Hanyang University, Ansan, 15588, South Korea.
Yi Eve SunStem Cell Translational Research Center, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Tian-Lin ChengState Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science, Institute for Translational Brain Research, Fudan University, Shanghai, 200032, China. chengtianlin@fudan.edu.cn.
Jeffrey SchweitzerLaboratory for Regenerative Cell Therapy, Department of Neurosurgery, Massachusetts General Hospital, George A. ''Doc'' Lopez, Harvard Medical School, Boston, MA, 02114, USA. jschweitzer1@mgh.harvard.edu.
Bin SongLaboratory for Regenerative Cell Therapy, Department of Neurosurgery, Massachusetts General Hospital, George A. ''Doc'' Lopez, Harvard Medical School, Boston, MA, 02114, USA. bsong@mgh.harvard.edu.ORCID http://orcid.org/0000-0002-3177-1911

Funding

National Key Research and Development Program of China 2022YFE0139000
6 · The paper itself

Abstract

backgroundTransplantation of midbrain dopaminergic neurons (mDANs) derived from human pluripotent stem cells (hPSCs) represents a promising therapeutic approach for Parkinson's disease (PD), with several clinical trials currently in progress. However, the poor survival of grafted mDANs, in part due to inflammation triggered by surgical injury, poses significant challenges to both therapeutic efficacy and safety. In recent years, mesenchymal stem cells (MSCs) and their derivatives have played an important role in the field of stem cell therapy due to their easy accessibility and immunomodulatory properties. However, their potential role as an adjunct in cell therapy remains unclear. Therefore, this study aims to investigate the protective effects of conditioned medium (CM) derived from MSCs and the mechanisms of action by which it attenuates surgery-induced neuroinflammation and enhances the survival of transplanted mDANs.

methodsTo mimic the neuroinflammatory response caused by the surgical aspect of cell transplantation, transplantation medium alone (i.e. without cells) was injected into the striatum of male NOD SCID mice. The anti-inflammatory effects of MSC-CM in vivo were evaluated by assessing the activation of microglia and expression levels of pro-inflammatory cytokines. Next, an in vitro cell death model was established using IFN-γ and TNF-α stimulation. The protective effects of MSC-CM against IFN-γ and TNF-α-induced inflammatory injury in mDANs were assessed using immunofluorescence staining and TUNEL assay. To identify the active components and underlying mechanisms for the protective effects of MSC-CM, inhibitory treatments, miRNA sequencing, dual-luciferase reporter assay, and subsequent validation by qPCR and Western blotting were performed. Finally, MSC-CM was administered intranasally into male NOD SCID mice following mDAN transplantation to evaluate its protective effects on the grafted mDANs in vivo.

resultsMSC-CM suppressed neuroinflammation and significantly protected mDANs from inflammation-induced cell death via inhibition of TLR3/NF-κB/p53 signaling pathway in this model system. This protective effect was largely reproduced by treatment with a specific component of the MSC-CM, miR-143-3p. Overexpression of miR-143-3p further enhanced the protective effects and mechanisms of action of MSC-CM.

conclusionsThis study demonstrates that MSC-CM or its component miR-143-3p exert protective effects on mDANs against inflammatory injury, primarily by inhibiting the TLR3/NFκB/p53 signaling pathway.

Indexed as

Dopaminergic NeuronsMesenchymal Stem CellsMicroRNAsNeuroprotective AgentsToll-Like Receptor 3Tumor Suppressor Protein p53AnimalsCulture Media, ConditionedHumansMaleMiceMice, Inbred NODMice, SCIDNF-kappa BSignal TransductionCulture Media, ConditionedMicroRNAsNeuroprotective AgentsNF-kappa BToll-Like Receptor 3Tumor Suppressor Protein p53Dopaminergic neuronsMesenchymal stem cellsmiR-143-3pParkinson’s diseaseTLR3/NF-κB/p53 pathway

Identifiers

PMID42482158
PMCPMC13681769

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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.