Evidence map›Paper›PMID 41343546›Full record

ArticlePloS one2025

Exosomes from bone marrow mesenchymal stem cells protect melanocytes under vitiligo-related conditions through induction of NRF2/HO1 expression.

Xuecheng Sun, Bo Huang, Gaobo Ruan, Aie Xu

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Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Xuecheng SunDepartment of Dermatology, The Third People's Hospital of Hangzhou, Hangzhou, Zhejiang, P.R. China.
Bo HuangDepartment of Dermatology, The Third People's Hospital of Hangzhou, Hangzhou, Zhejiang, P.R. China.
Gaobo RuanDepartment of Dermatology, The Third People's Hospital of Hangzhou, Hangzhou, Zhejiang, P.R. China.
Aie XuDepartment of Dermatology, The Third People's Hospital of Hangzhou, Hangzhou, Zhejiang, P.R. China.ORCID https://orcid.org/0009-0001-9673-0766

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVitiligo, a chronic autoimmune disease linked to excess oxidative stress, can be temporarily improved. Bone marrow mesenchymal stem cells (BMSCs)-derived exosomes (BMSCs-Exos) have recently emerged as a promising novel therapeutic means for vitiligo.

methodsExosomes were isolated and characterized from BMSCs-conditioned medium. PIG3V cells and those transfected with NRF2 siRNA or negative control were cultured under normal conditions or exposure to hydrogen peroxide (H₂O₂) to induce oxidative stress, with addition of BMSCs-conditioned medium, conditioned medium from BMSCs pretreated with GW4869 (referred to as BMSCs-GW4869), or BMSCs-Exos. Cell viability, apoptosis, and oxidative stress parameters, including cellular glutathione (GSH)/oxidized glutathione (GSSG) ratio, superoxide dismutase (SOD), reactive oxygen species (ROS), and malondialdehyde (MDA), were assessed. The expression of Ki67, NRF2, HO1, BAC, and Bcl-2 was measured.

resultsBMSC-Exos significantly enhanced cell viability and reduced apoptosis and oxidative stress in H₂O₂-treated PIG3V cells. Simultaneously, BMSCs-Exos reversed H₂O₂-induced downregulation of Ki67, NRF2, HO1, and Bcl-2, and upregulation of BAX in PIG3V cells. Silencing NRF2 by siRNA in PIG3V cells prior to H2O2 treatment abolished the protective effect of BMSCs-Exos and decreased the HO1 expression.

conclusionsBMSCs-Exos protect melanocytes from vitiliog-related oxidative stress by mitigating oxidative damage through induction of NRF2/HO1 expression.

Indexed as

ExosomesHeme Oxygenase-1MelanocytesMesenchymal Stem CellsNF-E2-Related Factor 2VitiligoApoptosisCell SurvivalCulture Media, ConditionedGene Expression RegulationHumansHydrogen PeroxideOxidative StressCulture Media, ConditionedHeme Oxygenase-1HMOX1 protein, humanHydrogen PeroxideNFE2L2 protein, humanNF-E2-Related Factor 2

Identifiers

PMID41343546
PMCPMC12677447

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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.