Erythrocytes from patients with ST-elevation myocardial infarction induce cardioprotection through the purinergic P2Y


Journal

Basic research in cardiology
ISSN: 1435-1803
Titre abrégé: Basic Res Cardiol
Pays: Germany
ID NLM: 0360342

Informations de publication

Date de publication:
16 09 2022
Historique:
received: 22 09 2021
accepted: 06 09 2022
revised: 05 09 2022
entrez: 16 9 2022
pubmed: 17 9 2022
medline: 21 9 2022
Statut: epublish

Résumé

Red blood cells (RBCs) are suggested to play a role in cardiovascular regulation by exporting nitric oxide (NO) bioactivity and ATP under hypoxia. It remains unknown whether such beneficial effects of RBCs are protective in patients with acute myocardial infarction. We investigated whether RBCs from patients with ST-elevation myocardial infarction (STEMI) protect against myocardial ischemia-reperfusion injury and whether such effect involves NO and purinergic signaling in the RBCs. RBCs from patients with STEMI undergoing primary coronary intervention and healthy controls were administered to isolated rat hearts subjected to global ischemia and reperfusion. Compared to RBCs from healthy controls, RBCs from STEMI patients reduced myocardial infarct size (30 ± 12% RBC healthy vs. 11 ± 5% RBC STEMI patients, P < 0.001), improved recovery of left-ventricular developed pressure and dP/dt and reduced left-ventricular end-diastolic pressure in hearts subjected to ischemia-reperfusion. Inhibition of RBC NO synthase with L-NAME or soluble guanylyl cyclase (sGC) with ODQ, and inhibition of cardiac protein kinase G (PKG) abolished the cardioprotective effect. Furthermore, the non-selective purinergic P2 receptor antagonist PPADS but not the P1 receptor antagonist 8PT attenuated the cardioprotection induced by RBCs from STEMI patients. The P2Y

Identifiants

pubmed: 36112326
doi: 10.1007/s00395-022-00953-4
pii: 10.1007/s00395-022-00953-4
pmc: PMC9481504
doi:

Substances chimiques

P2RY13 protein, human 0
Purinergic P2 Receptor Antagonists 0
Receptors, Purinergic P2 0
Nitric Oxide 31C4KY9ESH
Adenosine Triphosphate 8L70Q75FXE
Nitric Oxide Synthase EC 1.14.13.39
Cyclic GMP-Dependent Protein Kinases EC 2.7.11.12
Soluble Guanylyl Cyclase EC 4.6.1.2
NG-Nitroarginine Methyl Ester V55S2QJN2X

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

46

Informations de copyright

© 2022. The Author(s).

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Auteurs

Tong Jiao (T)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden. tong.jiao@ki.se.

Aida Collado (A)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden.

Ali Mahdi (A)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden.

Juliane Jurga (J)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden.
Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden.

John Tengbom (J)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden.

Nawzad Saleh (N)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden.
Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden.

Dinos Verouhis (D)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden.
Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden.

Felix Böhm (F)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden.
Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden.

Zhichao Zhou (Z)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden.

Jiangning Yang (J)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden.

John Pernow (J)

Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden. john.pernow@ki.se.
Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden. john.pernow@ki.se.

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