Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels

Mendez, Diego; Arauna, Diego; Fuentes, Francisco; Araya-Maturana, Ramiro; Palomo, Ivan; Alarcon, Marcelo; Sebastian, David; Zorzano, Antonio; FUENTES, EDUARDO

Abstract

Platelet activation plays a key role in cardiovascular diseases. The generation of mitochondrial reactive oxygen species (ROS) has been described as a critical step required for platelet activation. For this reason, it is necessary to find new molecules with antiplatelet activity and identify their mechanisms of action. Mitoquinone (MitoQ) is a mitochondria-targeted antioxidant that reduces mitochondrial overproduction of ROS. In this work, the antiplatelet effect of MitoQ through platelet adhesion and spreading, secretion, and aggregation was evaluated. Thus MitoQ, in a non-toxic effect, decreased platelet adhesion and spreading on collagen surface, and expression of P-selectin and CD63, and inhibited platelet aggregation induced by collagen, convulxin, thrombin receptor activator peptide-6 (TRAP-6), and phorbol 12-myristate 13-acetate (PMA). As an antiplatelet mechanism, we showed that MitoQ produced mitochondrial depolarization and decreased ATP secretion. Additionally, in platelets stimulated with antimycin A and collagen MitoQ significantly decreased ROS production. Our findings showed, for the first time, an antiplatelet effect of MitoQ that is probably associated with its mitochondrial antioxidant effect.

Más información

Título según WOS: Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels
Título de la Revista: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volumen: 21
Número: 17
Editorial: MDPI
Fecha de publicación: 2020
DOI:

10.3390/ijms21176192

Notas: ISI