Transfer of Cardiac Mitochondria Improves the Therapeutic Efficacy of Mesenchymal Stem Cells in a Preclinical Model of Ischemic Heart Disease.


Journal

Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052

Informations de publication

Date de publication:
11 02 2023
Historique:
received: 16 12 2022
revised: 31 01 2023
accepted: 08 02 2023
entrez: 25 2 2023
pubmed: 26 2 2023
medline: 3 3 2023
Statut: epublish

Résumé

The use of mesenchymal stem cells (MSCs) appears to be a promising therapeutic approach for cardiac repair after myocardial infarction. However, clinical trials have revealed the need to improve their therapeutic efficacy. Recent evidence demonstrated that mitochondria undergo spontaneous transfer from damaged cells to MSCs, resulting in the activation of the cytoprotective and pro-angiogenic functions of recipient MSCs. Based on these observations, we investigated whether the preconditioning of MSCs with mitochondria could optimize their therapeutic potential for ischemic heart disease. Human MSCs were exposed to mitochondria isolated from human fetal cardiomyocytes. After 24 h, the effects of mitochondria preconditioning on the MSCs' function were analyzed both in vitro and in vivo. We found that cardiac mitochondria-preconditioning improved the proliferation and repair properties of MSCs in vitro. Mechanistically, cardiac mitochondria mediate their stimulatory effects through the production of reactive oxygen species, which trigger their own degradation in recipient MSCs. These effects were further confirmed in vivo, as the mitochondria preconditioning of MSCs potentiated their therapeutic efficacy on cardiac function following their engraftment into infarcted mouse hearts. The preconditioning of MSCs with the artificial transfer of cardiac mitochondria appears to be promising strategy to improve the efficacy of MSC-based cell therapy in ischemic heart disease.

Sections du résumé

BACKGROUND
The use of mesenchymal stem cells (MSCs) appears to be a promising therapeutic approach for cardiac repair after myocardial infarction. However, clinical trials have revealed the need to improve their therapeutic efficacy. Recent evidence demonstrated that mitochondria undergo spontaneous transfer from damaged cells to MSCs, resulting in the activation of the cytoprotective and pro-angiogenic functions of recipient MSCs. Based on these observations, we investigated whether the preconditioning of MSCs with mitochondria could optimize their therapeutic potential for ischemic heart disease.
METHODS
Human MSCs were exposed to mitochondria isolated from human fetal cardiomyocytes. After 24 h, the effects of mitochondria preconditioning on the MSCs' function were analyzed both in vitro and in vivo.
RESULTS
We found that cardiac mitochondria-preconditioning improved the proliferation and repair properties of MSCs in vitro. Mechanistically, cardiac mitochondria mediate their stimulatory effects through the production of reactive oxygen species, which trigger their own degradation in recipient MSCs. These effects were further confirmed in vivo, as the mitochondria preconditioning of MSCs potentiated their therapeutic efficacy on cardiac function following their engraftment into infarcted mouse hearts.
CONCLUSIONS
The preconditioning of MSCs with the artificial transfer of cardiac mitochondria appears to be promising strategy to improve the efficacy of MSC-based cell therapy in ischemic heart disease.

Identifiants

pubmed: 36831249
pii: cells12040582
doi: 10.3390/cells12040582
pmc: PMC9953768
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

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Auteurs

Marie-Luce Vignais (ML)

Institut de Génomique Fonctionnelle, University Montpellier, CNRS, INSERM, 34094 Montpellier, France.

Jennyfer Levoux (J)

Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France.
Sorbonne Université, Institut de Biologie Paris-Seine (IBPS), CNRS UMR 8256, INSERM U1164, Biological Adaptation and Ageing, 75005 Paris, France.

Pierre Sicard (P)

PhyMedExp, Inserm, CNRS, University of Montpellier, 34295 Montpellier, France.

Khattar Khattar (K)

Institut de Génomique Fonctionnelle, University Montpellier, CNRS, INSERM, 34094 Montpellier, France.

Catherine Lozza (C)

PhyMedExp, Inserm, CNRS, University of Montpellier, 34295 Montpellier, France.

Marianne Gervais (M)

Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France.

Safia Mezhoud (S)

Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France.

Jean Nakhle (J)

Institut de Génomique Fonctionnelle, University Montpellier, CNRS, INSERM, 34094 Montpellier, France.

Frederic Relaix (F)

Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France.
École Nationale Vétérinaire d'Alfort, IMRB, 94700 Maisons-Alfort, France.
APHP, Hôpitaux Universitaires Henri Mondor & Centre de Référence des Maladies Neuromusculaires GNMH, 94000 Créteil, France.

Onnik Agbulut (O)

Sorbonne Université, Institut de Biologie Paris-Seine (IBPS), CNRS UMR 8256, INSERM U1164, Biological Adaptation and Ageing, 75005 Paris, France.

Jeremy Fauconnier (J)

PhyMedExp, Inserm, CNRS, University of Montpellier, 34295 Montpellier, France.

Anne-Marie Rodriguez (AM)

Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France.
Sorbonne Université, Institut de Biologie Paris-Seine (IBPS), CNRS UMR 8256, INSERM U1164, Biological Adaptation and Ageing, 75005 Paris, France.
APHP, Hôpitaux Universitaires Henri Mondor & Centre de Référence des Maladies Neuromusculaires GNMH, 94000 Créteil, France.

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Classifications MeSH