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

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...
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Autor*in:	Diego Méndez [verfasserIn] Diego Arauna [verfasserIn] Francisco Fuentes [verfasserIn] Ramiro Araya-Maturana [verfasserIn] Iván Palomo [verfasserIn] Marcelo Alarcón [verfasserIn] David Sebastián [verfasserIn] Antonio Zorzano [verfasserIn] Eduardo Fuentes [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	mitoquinone mitochondria platelets ROS MitoQ

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 21(2020), 17, p 6192
Übergeordnetes Werk:	volume:21 ; year:2020 ; number:17, p 6192

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.3390/ijms21176192

Katalog-ID:	DOAJ04631668X

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allfieldsSound	10.3390/ijms21176192 doi (DE-627)DOAJ04631668X (DE-599)DOAJ6dbfa5740a2848d295dfdfb2965f2eb8 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Diego Méndez verfasserin aut Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. mitoquinone mitochondria platelets ROS MitoQ Biology (General) Chemistry Diego Arauna verfasserin aut Francisco Fuentes verfasserin aut Ramiro Araya-Maturana verfasserin aut Iván Palomo verfasserin aut Marcelo Alarcón verfasserin aut David Sebastián verfasserin aut Antonio Zorzano verfasserin aut Eduardo Fuentes verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 21(2020), 17, p 6192 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:21 year:2020 number:17, p 6192 https://doi.org/10.3390/ijms21176192 kostenfrei https://doaj.org/article/6dbfa5740a2848d295dfdfb2965f2eb8 kostenfrei https://www.mdpi.com/1422-0067/21/17/6192 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2020 17, p 6192
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source	In International Journal of Molecular Sciences 21(2020), 17, p 6192 volume:21 year:2020 number:17, p 6192
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callnumber-first	Q - Science
author	Diego Méndez
spellingShingle	Diego Méndez misc QH301-705.5 misc QD1-999 misc mitoquinone misc mitochondria misc platelets misc ROS misc MitoQ misc Biology (General) misc Chemistry Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels
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topic_title	QH301-705.5 QD1-999 Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels mitoquinone mitochondria platelets ROS MitoQ
topic	misc QH301-705.5 misc QD1-999 misc mitoquinone misc mitochondria misc platelets misc ROS misc MitoQ misc Biology (General) misc Chemistry
topic_unstemmed	misc QH301-705.5 misc QD1-999 misc mitoquinone misc mitochondria misc platelets misc ROS misc MitoQ misc Biology (General) misc Chemistry
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title	Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels
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title_full	Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels
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author_browse	Diego Méndez Diego Arauna Francisco Fuentes Ramiro Araya-Maturana Iván Palomo Marcelo Alarcón David Sebastián Antonio Zorzano Eduardo Fuentes
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title_sort	mitoquinone (mitoq) inhibits platelet activation steps by reducing ros levels
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title_auth	Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels
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.
abstractGer	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.
abstract_unstemmed	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.
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container_issue	17, p 6192
title_short	Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels
url	https://doi.org/10.3390/ijms21176192 https://doaj.org/article/6dbfa5740a2848d295dfdfb2965f2eb8 https://www.mdpi.com/1422-0067/21/17/6192 https://doaj.org/toc/1661-6596 https://doaj.org/toc/1422-0067
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author2	Diego Arauna Francisco Fuentes Ramiro Araya-Maturana Iván Palomo Marcelo Alarcón David Sebastián Antonio Zorzano Eduardo Fuentes
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up_date	2024-07-03T19:58:19.661Z
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Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels

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