Extracellular vesicles from human cardiac stromal cells up-regulate cardiomyocyte protective responses to hypoxia.


Journal

Stem cell research & therapy
ISSN: 1757-6512
Titre abrégé: Stem Cell Res Ther
Pays: England
ID NLM: 101527581

Informations de publication

Date de publication:
12 Oct 2024
Historique:
received: 27 08 2024
accepted: 07 10 2024
medline: 13 10 2024
pubmed: 13 10 2024
entrez: 12 10 2024
Statut: epublish

Résumé

Cell therapy can protect cardiomyocytes from hypoxia, primarily via paracrine secretions, including extracellular vesicles (EVs). Since EVs fulfil specific biological functions based on their cellular origin, we hypothesised that EVs from human cardiac stromal cells (CMSCLCs) obtained from coronary artery bypass surgery may have cardioprotective properties. This study characterises CMSCLC EVs (C_EVs), miRNA cargo, cardioprotective efficacy and transcriptomic modulation of hypoxic human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). C_EVs are compared to bone marrow mesenchymal stromal cell EVs (B_EVs) which are a known therapeutic EV type. Cells were characterised for surface markers, gene expression and differentiation potential. EVs were compared for yield, phenotype, and ability to protect hiPSC-CMs from hypoxia/reoxygenation injury. EV dose was normalised by both protein concentration and particle count, allowing direct comparison. C_EV and B_EV miRNA cargo was profiled and RNA-seq was performed on EV-treated hypoxic hiPSC-CMs, then data were integrated by multi-omics. Confirmatory experiments were carried out using miRNA mimics. At the same dose, C_EVs were more effective than B_EVs at protecting CM integrity, reducing apoptotic markers, and cell death during hypoxia. While C_EVs and B_EVs shared 70-77% similarity in miRNA content, C_EVs contained unique miRNAs, including miR-202-5p, miR-451a and miR-142-3p. Delivering miRNA mimics confirmed that miR-1260a and miR-202/451a/142 were cardioprotective, and the latter upregulated protective pathways similar to whole C_EVs. This study demonstrates the potential of cardiac tissues, routinely discarded following surgery, as a valuable source of EVs for myocardial infarction therapy. We also identify miR-1260a as protective of CM hypoxia.

Sections du résumé

BACKGROUND BACKGROUND
Cell therapy can protect cardiomyocytes from hypoxia, primarily via paracrine secretions, including extracellular vesicles (EVs). Since EVs fulfil specific biological functions based on their cellular origin, we hypothesised that EVs from human cardiac stromal cells (CMSCLCs) obtained from coronary artery bypass surgery may have cardioprotective properties.
OBJECTIVES OBJECTIVE
This study characterises CMSCLC EVs (C_EVs), miRNA cargo, cardioprotective efficacy and transcriptomic modulation of hypoxic human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). C_EVs are compared to bone marrow mesenchymal stromal cell EVs (B_EVs) which are a known therapeutic EV type.
METHODS METHODS
Cells were characterised for surface markers, gene expression and differentiation potential. EVs were compared for yield, phenotype, and ability to protect hiPSC-CMs from hypoxia/reoxygenation injury. EV dose was normalised by both protein concentration and particle count, allowing direct comparison. C_EV and B_EV miRNA cargo was profiled and RNA-seq was performed on EV-treated hypoxic hiPSC-CMs, then data were integrated by multi-omics. Confirmatory experiments were carried out using miRNA mimics.
RESULTS RESULTS
At the same dose, C_EVs were more effective than B_EVs at protecting CM integrity, reducing apoptotic markers, and cell death during hypoxia. While C_EVs and B_EVs shared 70-77% similarity in miRNA content, C_EVs contained unique miRNAs, including miR-202-5p, miR-451a and miR-142-3p. Delivering miRNA mimics confirmed that miR-1260a and miR-202/451a/142 were cardioprotective, and the latter upregulated protective pathways similar to whole C_EVs.
CONCLUSIONS CONCLUSIONS
This study demonstrates the potential of cardiac tissues, routinely discarded following surgery, as a valuable source of EVs for myocardial infarction therapy. We also identify miR-1260a as protective of CM hypoxia.

Identifiants

pubmed: 39396003
doi: 10.1186/s13287-024-03983-y
pii: 10.1186/s13287-024-03983-y
doi:

Substances chimiques

MicroRNAs 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

363

Subventions

Organisme : National Science and Technology Council (TW)
ID : 112-2636-B-038-005
Organisme : Office of Research and Development, Taipei Medical University
ID : 112-3805-006-111

Informations de copyright

© 2024. The Author(s).

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Auteurs

Andreas Czosseck (A)

Graduate Institute of Biomedical Materials & Tissue Engineering, College of Biomedical Engineering, Taipei Medical University, 301 Yuantong Road, Taipei, 235603, Taiwan.

Max M Chen (MM)

Graduate Institute of Biomedical Materials & Tissue Engineering, College of Biomedical Engineering, Taipei Medical University, 301 Yuantong Road, Taipei, 235603, Taiwan.

Chuan-Chih Hsu (CC)

Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, 250 Wuxing Street, Taipei, 110, Taiwan.
Division of Cardiovascular Surgery, Department of Surgery, Taipei Medical University Hospital, 250 Wuxing Street, Taipei, 110, Taiwan.

Gleb Shamrin (G)

Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, 250 Wuxing Street, Taipei, 110, Taiwan.

Annette Meeson (A)

Biosciences Institute, Newcastle University, Newcastle upon Tyne, NE1 3BZ, UK.

Rachel Oldershaw (R)

Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, Faculty of Health and Life Sciences, University of Liverpool, William Henry Duncan Building, 6 West Derby Street, Liverpool, L7 8TX, UK.

Helen Nguyen (H)

Graduate Institute of Biomedical Materials & Tissue Engineering, College of Biomedical Engineering, Taipei Medical University, 301 Yuantong Road, Taipei, 235603, Taiwan.

Dora Livkisa (D)

International PhD Program in Biomedical Engineering, College of Biomedical Engineering, Taipei Medical University, 301 Yuantong Road, Taipei, 235603, Taiwan.

David J Lundy (DJ)

Graduate Institute of Biomedical Materials & Tissue Engineering, College of Biomedical Engineering, Taipei Medical University, 301 Yuantong Road, Taipei, 235603, Taiwan. dlundy@tmu.edu.tw.
International PhD Program in Biomedical Engineering, College of Biomedical Engineering, Taipei Medical University, 301 Yuantong Road, Taipei, 235603, Taiwan. dlundy@tmu.edu.tw.
Center for Cell Therapy, Taipei Medical University Hospital, 250 Wuxing Street, Taipei, 110, Taiwan. dlundy@tmu.edu.tw.
College of Biomedical Engineering, 301 Yuantong Road, Taipei, 235605, Taiwan. dlundy@tmu.edu.tw.

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