Plasma-derived extracellular vesicles from myocardial infarction patients inhibits tumor necrosis factor-alpha induced cardiac cell death - 02/03/22
, Bertil Lindahl a, Sara Bergström Lind c, d, Ganna Shevchenko c, Agneta Siegbahn b, Christina Christersson aBienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
| pages | 13 |
| Iconographies | 6 |
| Vidéos | 0 |
| Autres | 0 |
Abstract |
Rationale |
Extracellular vesicles (EVs) derived exogenously from pluripotent stem cells or endogenously from healthy human serum exert cardioprotective effects after injury. However role of endogenous EVs from myocardial infarction (MI) patients not well understood in this settings.
Methods and results |
The EVs from plasma of MI patients with preserved or reduced left ventricular ejection fraction (LVEF) and healthy controls (HC) were purified and characterized by flow cytometry, mass spectrometry (MS) and transmission electron microscopy (TEM). HCM and human cardiac microvascular endothelial cells (hCMVECs), under individual culture or co-culture, were used to study functional effects of EVs upon TNFα stimulation. These effects of EVs on HCM and hCMVECs were observed using cell death assays, western blots and confocal microscopy. Higher concentrations of platelet-, leukocyte-, endothelial- and erythrocyte-derived EVs were found in MI patients, both with preserved and reduced LVEF, compared to HC, and MS data on MI EVs proteome displayed alteration in several proteins. MI EVs protected HCM and hCMVECs against staurosporine-induced apoptosis. Furthermore, MI EVs were observed to abrogate TNFα-triggered HCM and hCMVECs death under both individually cultured and co-cultured conditions. MI EVs failed to inhibit TNFα induced hCMVECs and HCM activation when cultured individually, however co-cultured hCMVECs with HCM supported MI EVs capacity to attenuate TNFα induced cells activation. MI CD41+ EVs but not HC EVs were found to be internalized by HCM directly or migrated through hCMVECs to HCM. MI EVs indirectly restores TNFα mediated drop in mitochondrial membrane potential.
Conclusions |
Endogenous EVs from MI patients, regardless of severity of the MI exert cardioprotective potential upon TNFα-induced cell death. Patient-derived EVs needs to be further explored to elucidate their potential cardioprotective role during MI.
Le texte complet de cet article est disponible en PDF.Keywords : Extracellular vesicles, Myocardial infarction, Cardiomyocytes, Tumor necrosis factor alpha, Apoptosis
Abbreviations : EVs, TNFα, hCMVECs, HCM, MI, LVEF
Plan
Vol 70 - N° 2
Article 103323- mai 2022 Retour au numéro
Article précédent
- Immune restoration therapy for multidrug-resistant CMV disease in an allogenic stem cell transplant recipient
- Olivier Paccoud, Sophie Alain, Joel Gozlan, Sabrine Jarboui, David Boutolleau, Sébastien Hantz, Giorgia Battipaglia, Annalisa Paviglianiti, Rémy Duléry, Florent Malard, Clémence Médiavilla, Simona Sestili, Béatrice Gaugler, Jean-Luc Meynard, Jérôme Pacanowski, Mohamad Mohty, Eolia Brissot
- Allogeneic adipose-derived mesenchymal stromal cell transplantation for refractory lupus nephritis: Results of a phase I clinical trial
- Amin Ranjbar, Halimeh Hassanzadeh, Faezeh Jahandoust, Raheleh Miri, Hamid Reza Bidkhori, Seyed Mostafa Monzavi, Nasser Sanjar-Moussavi, Maryam M. Matin, Zhaleh Shariati-Sarabi
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’achat d’article à l’unité est indisponible à l’heure actuelle.
Déjà abonné à cette revue ?