Mesenchymal stem cell-mediated mitochondrial transfer regulates the fate of B lymphocytes

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F86652036%3A_____%2F25%3A00647610" target="_blank" >RIV/86652036:_____/25:00647610 - isvavai.cz</a>

Alternative codes found

RIV/00216208:11110/25:10505714 RIV/00216208:11310/25:10505714

Result on the web

<a href="https://onlinelibrary.wiley.com/doi/epdf/10.1111/eci.70073" target="_blank" >https://onlinelibrary.wiley.com/doi/epdf/10.1111/eci.70073</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/eci.70073" target="_blank" >10.1111/eci.70073</a>

Result language

angličtina

Original language name

Mesenchymal stem cell-mediated mitochondrial transfer regulates the fate of B lymphocytes

Original language description

BackgroundMitochondrial transfer is becoming recognized as an important immunomodulatory mechanism used by mesenchymal stem cells (MSCs) to influence immune cells. While effects on T cells and macrophages have been documented, the influence on B cells remains unexplored. This study investigates the modulation of B lymphocyte fate by MSC-mediated mitochondrial transfer.MethodsMSCs labelled with MitoTracker dyes or derived from mito::mKate2 transgenic mice were co-cultured with splenocytes. Flow cytometry assessed mitochondrial transfer, reactive oxygen species (ROS) levels, apoptosis and mitophagy. Glucose uptake was measured using the 2-NBDG assay. RNA sequencing analysed gene expression changes in CD19+ mitochondria recipients and nonrecipients. Pathway analysis identified affected processes. In an LPS-induced inflammation model, mito::mKate2 MSCs were administered, and B cells from different organs were analysed for mitochondrial uptake and phenotypic changes. MSC-derived mitochondria were also isolated to confirm uptake by FACS-sorted CD19+ cells.ResultsMSCs transferred mitochondria to CD19+ cells, though less than to other immune cells. Transfer correlated with ROS levels and mitophagy induction. Mitochondria were preferentially acquired by activated B cells, as indicated by increased CD69 expression and glycolytic activity. Bidirectional transfer occurred, with immune cells exchanging dysfunctional mitochondria for functional ones. CD19+ recipients exhibited increased viability, proliferation and altered gene expression, with upregulated cell division genes and downregulated antigen presentation genes. In vivo, mitochondrial acquisition reduced B cell activation and inflammatory cytokine production. Pre-sorted B cells also acquired isolated mitochondria, exhibiting a similar anti-inflammatory phenotype.ConclusionsThese findings highlight mitochondrial trafficking as a key MSC-immune cell interaction mechanism with immunomodulatory therapeutic potential.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

30218 - General and internal medicine

Project

<a href="/en/project/GX21-04607X" target="_blank" >GX21-04607X: Horizontal transfer of mitochondria in cancer biology</a><br>

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2025

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

European Journal of Clinical Investigation

ISSN

0014-2972

e-ISSN

1365-2362

Volume of the periodical

55

Issue of the periodical within the volume

10

Country of publishing house

US - UNITED STATES

Number of pages

19

Pages from-to

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UT code for WoS article

001488342900001

EID of the result in the Scopus database

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