RapamycinFungusV1, Main, Exploration, bibRecord, 000493

Sin1 (Stress-Activated Protein Kinase-Interacting Protein) Regulates Ischemia-Induced Microthrombosis Through Integrin αIIbβ3-Mediated Outside-In Signaling and Hypoxia Responses in Platelets.

Identifieur interne : 000493 ( Main/Exploration ); précédent : 000492; suivant : 000494

Sin1 (Stress-Activated Protein Kinase-Interacting Protein) Regulates Ischemia-Induced Microthrombosis Through Integrin αIIbβ3-Mediated Outside-In Signaling and Hypoxia Responses in Platelets.

Source :

Arteriosclerosis, thrombosis, and vascular biology [ 1524-4636 ] ; 2018.

RBID : pubmed:30571167

Descripteurs français

English descriptors

KwdEn :
- Adaptor Proteins, Signal Transducing (blood), Adult (MeSH), Aged (MeSH), Aged, 80 and over (MeSH), Animals (MeSH), Blood Platelets (enzymology), Carrier Proteins (blood), Carrier Proteins (genetics), Cell Hypoxia (MeSH), Disease Models, Animal (MeSH), Female (MeSH), Humans (MeSH), Male (MeSH), Mechanistic Target of Rapamycin Complex 2 (metabolism), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Middle Aged (MeSH), Myocardial Infarction (complications), Phosphorylation (MeSH), Platelet Activation (MeSH), Platelet Glycoprotein GPIIb-IIIa Complex (metabolism), Proto-Oncogene Proteins c-akt (blood), Reactive Oxygen Species (blood), Signal Transduction (MeSH), Sirtuin 3 (blood), Sirtuin 3 (genetics), Superoxide Dismutase (blood), Superoxide Dismutase (genetics), Thrombosis (blood), Thrombosis (enzymology), Thrombosis (genetics), Thrombosis (prevention & control).
MESH :
- chemical , blood : Adaptor Proteins, Signal Transducing, Carrier Proteins, Proto-Oncogene Proteins c-akt, Reactive Oxygen Species, Sirtuin 3, Superoxide Dismutase.
- blood : Thrombosis.
- complications : Myocardial Infarction.
- enzymology : Blood Platelets, Thrombosis.
- chemical , genetics : Carrier Proteins, Sirtuin 3, Superoxide Dismutase, Thrombosis.
- chemical , metabolism : Mechanistic Target of Rapamycin Complex 2, Platelet Glycoprotein GPIIb-IIIa Complex.
- prevention & control : Thrombosis.
- Adult, Aged, Aged, 80 and over, Animals, Cell Hypoxia, Disease Models, Animal, Female, Humans, Male, Mice, Inbred C57BL, Mice, Knockout, Middle Aged, Phosphorylation, Platelet Activation, Signal Transduction.

Abstract

Objective- Microthrombosis as a serious consequence of myocardial infarction, impairs the microvascular environment and increases the occurrences of heart failure, arrhythmia, and death. Sin1 (stress-activated protein kinase-interacting protein) as an essential component of mTORC2 (mammalian target of rapamycin complex 2) is required for cell proliferation and metabolism in response to nutrients, stress, and reactive oxygen species and activates Akt and PKC (protein kinase C). However, the activation and function of Sin1/mTORC2 in ischemia-induced microthrombosis remain poorly understood. Approach and Results- The phosphorylation of the mTORC2 target Akt at S473 (serine 473) was significantly elevated in platelets from the distal end of left anterior descending obstructions from patients who underwent off-pump coronary artery bypass grafting compared with platelets from healthy subjects. Consistent with this finding, phosphorylation of T86 in Sin1 was also dramatically increased. Importantly, the augmented levels of phosphorylated Sin1 and Akt in platelets from 61 preoperative patients with ST-segment-elevation myocardial infarction correlated well with the no-reflow phenomena observed after revascularization. Platelet-specific Sin1 deficiency mice and Sin1 T86 phosphorylation deficiency mice were established to explore the underlying mechanisms in platelet activation. Mechanistically, Sin1 T86 phosphorylation amplifies mTORC2-mediated downstream signals; it is also required for αIIbβ3-mediated outside-in signaling and plays a role in generating hypoxia/reactive oxygen species through NAD⁺/Sirt3 (sirtuin 3)/SOD2 (superoxide dismutase 2) pathway. Importantly, Sin1 deletion in platelets protected mice from ischemia-induced microvascular embolization and subsequent heart dysfunction in a mouse model of myocardial infarction. Conclusions- Together, the results of our study reveal a novel role for Sin1 in platelet activation. Thus, Sin1 may be a valuable therapeutic target for interventions for ischemia-induced myocardial infarction deterioration.

DOI: 10.1161/ATVBAHA.118.311822
PubMed: 30571167

Affiliations:

République populaire de Chine

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<author><name sortKey="Xu, Yanyan" sort="Xu, Yanyan" uniqKey="Xu Y" first="Yanyan" last="Xu">Yanyan Xu</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Yan, Lichong" sort="Yan, Lichong" uniqKey="Yan L" first="Lichong" last="Yan">Lichong Yan</name>
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</author>
<author><name sortKey="Zhang, Mingliang" sort="Zhang, Mingliang" uniqKey="Zhang M" first="Mingliang" last="Zhang">Mingliang Zhang</name>
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<author><name sortKey="Hu, Zhenlei" sort="Hu, Zhenlei" uniqKey="Hu Z" first="Zhenlei" last="Hu">Zhenlei Hu</name>
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<wicri:noCountry code="subField">Z.H.).</wicri:noCountry>
</affiliation>
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<author><name sortKey="Gu, Jianmin" sort="Gu, Jianmin" uniqKey="Gu J" first="Jianmin" last="Gu">Jianmin Gu</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiovascular Surgery, Renji Hospital (J.G., S.X.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Fan, Xuemei" sort="Fan, Xuemei" uniqKey="Fan X" first="Xuemei" last="Fan">Xuemei Fan</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Zhang, Lin" sort="Zhang, Lin" uniqKey="Zhang L" first="Lin" last="Zhang">Lin Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Zhang, Junfeng" sort="Zhang, Junfeng" uniqKey="Zhang J" first="Junfeng" last="Zhang">Junfeng Zhang</name>
</author>
<author><name sortKey="Xue, Song" sort="Xue, Song" uniqKey="Xue S" first="Song" last="Xue">Song Xue</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Cardiovascular Surgery, Renji Hospital (J.G., S.X.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiovascular Surgery, Renji Hospital (J.G., S.X.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Chen, Guoqiang" sort="Chen, Guoqiang" uniqKey="Chen G" first="Guoqiang" last="Chen">Guoqiang Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology (G.C.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology (G.C.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name>
<affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Liu, Junling" sort="Liu, Junling" uniqKey="Liu J" first="Junling" last="Liu">Junling Liu</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
<affiliation><nlm:affiliation>Collaborative Innovation Center of Hematology, Soochow University, China (J.L.).</nlm:affiliation>
<wicri:noCountry code="subField">China (J.L.).</wicri:noCountry>
</affiliation>
</author>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Sin1 (Stress-Activated Protein Kinase-Interacting Protein) Regulates Ischemia-Induced Microthrombosis Through Integrin αIIbβ3-Mediated Outside-In Signaling and Hypoxia Responses in Platelets.</title>
<author><name sortKey="Xu, Yanyan" sort="Xu, Yanyan" uniqKey="Xu Y" first="Yanyan" last="Xu">Yanyan Xu</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Ouyang, Xinxing" sort="Ouyang, Xinxing" uniqKey="Ouyang X" first="Xinxing" last="Ouyang">Xinxing Ouyang</name>
<affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Yan, Lichong" sort="Yan, Lichong" uniqKey="Yan L" first="Lichong" last="Yan">Lichong Yan</name>
<affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Zhang, Mingliang" sort="Zhang, Mingliang" uniqKey="Zhang M" first="Mingliang" last="Zhang">Mingliang Zhang</name>
<affiliation><nlm:affiliation>Department of Cardiology, Shanghai Jiao Tong University School of Medicine Affiliated Ninth People's Hospital, Shanghai, China (M.Z., Z.H.).</nlm:affiliation>
<wicri:noCountry code="subField">Z.H.).</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Hu, Zhenlei" sort="Hu, Zhenlei" uniqKey="Hu Z" first="Zhenlei" last="Hu">Zhenlei Hu</name>
<affiliation><nlm:affiliation>Department of Cardiology, Shanghai Jiao Tong University School of Medicine Affiliated Ninth People's Hospital, Shanghai, China (M.Z., Z.H.).</nlm:affiliation>
<wicri:noCountry code="subField">Z.H.).</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Gu, Jianmin" sort="Gu, Jianmin" uniqKey="Gu J" first="Jianmin" last="Gu">Jianmin Gu</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Cardiovascular Surgery, Renji Hospital (J.G., S.X.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiovascular Surgery, Renji Hospital (J.G., S.X.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Fan, Xuemei" sort="Fan, Xuemei" uniqKey="Fan X" first="Xuemei" last="Fan">Xuemei Fan</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Zhang, Lin" sort="Zhang, Lin" uniqKey="Zhang L" first="Lin" last="Zhang">Lin Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Zhang, Junfeng" sort="Zhang, Junfeng" uniqKey="Zhang J" first="Junfeng" last="Zhang">Junfeng Zhang</name>
</author>
<author><name sortKey="Xue, Song" sort="Xue, Song" uniqKey="Xue S" first="Song" last="Xue">Song Xue</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Cardiovascular Surgery, Renji Hospital (J.G., S.X.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiovascular Surgery, Renji Hospital (J.G., S.X.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Chen, Guoqiang" sort="Chen, Guoqiang" uniqKey="Chen G" first="Guoqiang" last="Chen">Guoqiang Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology (G.C.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology (G.C.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name>
<affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Liu, Junling" sort="Liu, Junling" uniqKey="Liu J" first="Junling" last="Liu">Junling Liu</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine</wicri:regionArea>
<wicri:noRegion>Shanghai Jiao Tong University School of Medicine</wicri:noRegion>
</affiliation>
<affiliation><nlm:affiliation>Collaborative Innovation Center of Hematology, Soochow University, China (J.L.).</nlm:affiliation>
<wicri:noCountry code="subField">China (J.L.).</wicri:noCountry>
</affiliation>
</author>
</analytic>
<series><title level="j">Arteriosclerosis, thrombosis, and vascular biology</title>
<idno type="eISSN">1524-4636</idno>
<imprint><date when="2018" type="published">2018</date>
</imprint>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (blood)</term>
<term>Adult (MeSH)</term>
<term>Aged (MeSH)</term>
<term>Aged, 80 and over (MeSH)</term>
<term>Animals (MeSH)</term>
<term>Blood Platelets (enzymology)</term>
<term>Carrier Proteins (blood)</term>
<term>Carrier Proteins (genetics)</term>
<term>Cell Hypoxia (MeSH)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Male (MeSH)</term>
<term>Mechanistic Target of Rapamycin Complex 2 (metabolism)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Middle Aged (MeSH)</term>
<term>Myocardial Infarction (complications)</term>
<term>Phosphorylation (MeSH)</term>
<term>Platelet Activation (MeSH)</term>
<term>Platelet Glycoprotein GPIIb-IIIa Complex (metabolism)</term>
<term>Proto-Oncogene Proteins c-akt (blood)</term>
<term>Reactive Oxygen Species (blood)</term>
<term>Signal Transduction (MeSH)</term>
<term>Sirtuin 3 (blood)</term>
<term>Sirtuin 3 (genetics)</term>
<term>Superoxide Dismutase (blood)</term>
<term>Superoxide Dismutase (genetics)</term>
<term>Thrombosis (blood)</term>
<term>Thrombosis (enzymology)</term>
<term>Thrombosis (genetics)</term>
<term>Thrombosis (prevention & control)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation plaquettaire (MeSH)</term>
<term>Adulte (MeSH)</term>
<term>Adulte d'âge moyen (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Complexe glycoprotéique IIb-IIIa de la membrane plaquettaire (métabolisme)</term>
<term>Complexe-2 cible mécanistique de la rapamycine (métabolisme)</term>
<term>Espèces réactives de l'oxygène (sang)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Hypoxie cellulaire (MeSH)</term>
<term>Infarctus du myocarde (complications)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Phosphorylation (MeSH)</term>
<term>Plaquettes (enzymologie)</term>
<term>Protéines adaptatrices de la transduction du signal (sang)</term>
<term>Protéines de transport (génétique)</term>
<term>Protéines de transport (sang)</term>
<term>Protéines proto-oncogènes c-akt (sang)</term>
<term>Sirtuine-3 (génétique)</term>
<term>Sirtuine-3 (sang)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Souris knockout (MeSH)</term>
<term>Sujet âgé (MeSH)</term>
<term>Sujet âgé de 80 ans ou plus (MeSH)</term>
<term>Superoxide dismutase (génétique)</term>
<term>Superoxide dismutase (sang)</term>
<term>Thrombose (enzymologie)</term>
<term>Thrombose (génétique)</term>
<term>Thrombose (prévention et contrôle)</term>
<term>Thrombose (sang)</term>
<term>Transduction du signal (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term>
<term>Carrier Proteins</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>Reactive Oxygen Species</term>
<term>Sirtuin 3</term>
<term>Superoxide Dismutase</term>
</keywords>
<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Thrombosis</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Myocardial Infarction</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Plaquettes</term>
<term>Thrombose</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Blood Platelets</term>
<term>Thrombosis</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Carrier Proteins</term>
<term>Sirtuin 3</term>
<term>Superoxide Dismutase</term>
<term>Thrombosis</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines de transport</term>
<term>Sirtuine-3</term>
<term>Superoxide dismutase</term>
<term>Thrombose</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Mechanistic Target of Rapamycin Complex 2</term>
<term>Platelet Glycoprotein GPIIb-IIIa Complex</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Complexe glycoprotéique IIb-IIIa de la membrane plaquettaire</term>
<term>Complexe-2 cible mécanistique de la rapamycine</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Thrombosis</term>
</keywords>
<keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Thrombose</term>
</keywords>
<keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Espèces réactives de l'oxygène</term>
<term>Infarctus du myocarde</term>
<term>Protéines adaptatrices de la transduction du signal</term>
<term>Protéines de transport</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Sirtuine-3</term>
<term>Superoxide dismutase</term>
<term>Thrombose</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Animals</term>
<term>Cell Hypoxia</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Middle Aged</term>
<term>Phosphorylation</term>
<term>Platelet Activation</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation plaquettaire</term>
<term>Adulte</term>
<term>Adulte d'âge moyen</term>
<term>Animaux</term>
<term>Femelle</term>
<term>Humains</term>
<term>Hypoxie cellulaire</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Phosphorylation</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Sujet âgé</term>
<term>Sujet âgé de 80 ans ou plus</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">Objective- Microthrombosis as a serious consequence of myocardial infarction, impairs the microvascular environment and increases the occurrences of heart failure, arrhythmia, and death. Sin1 (stress-activated protein kinase-interacting protein) as an essential component of mTORC2 (mammalian target of rapamycin complex 2) is required for cell proliferation and metabolism in response to nutrients, stress, and reactive oxygen species and activates Akt and PKC (protein kinase C). However, the activation and function of Sin1/mTORC2 in ischemia-induced microthrombosis remain poorly understood. Approach and Results- The phosphorylation of the mTORC2 target Akt at S473 (serine 473) was significantly elevated in platelets from the distal end of left anterior descending obstructions from patients who underwent off-pump coronary artery bypass grafting compared with platelets from healthy subjects. Consistent with this finding, phosphorylation of T86 in Sin1 was also dramatically increased. Importantly, the augmented levels of phosphorylated Sin1 and Akt in platelets from 61 preoperative patients with ST-segment-elevation myocardial infarction correlated well with the no-reflow phenomena observed after revascularization. Platelet-specific Sin1 deficiency mice and Sin1 T86 phosphorylation deficiency mice were established to explore the underlying mechanisms in platelet activation. Mechanistically, Sin1 T86 phosphorylation amplifies mTORC2-mediated downstream signals; it is also required for αIIbβ3-mediated outside-in signaling and plays a role in generating hypoxia/reactive oxygen species through NAD<sup>+</sup>
/Sirt3 (sirtuin 3)/SOD2 (superoxide dismutase 2) pathway. Importantly, Sin1 deletion in platelets protected mice from ischemia-induced microvascular embolization and subsequent heart dysfunction in a mouse model of myocardial infarction. Conclusions- Together, the results of our study reveal a novel role for Sin1 in platelet activation. Thus, Sin1 may be a valuable therapeutic target for interventions for ischemia-induced myocardial infarction deterioration.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30571167</PMID>
<DateCompleted><Year>2019</Year>
<Month>07</Month>
<Day>29</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>07</Month>
<Day>29</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1524-4636</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>38</Volume>
<Issue>12</Issue>
<PubDate><Year>2018</Year>
<Month>12</Month>
</PubDate>
</JournalIssue>
<Title>Arteriosclerosis, thrombosis, and vascular biology</Title>
<ISOAbbreviation>Arterioscler Thromb Vasc Biol</ISOAbbreviation>
</Journal>
<ArticleTitle>Sin1 (Stress-Activated Protein Kinase-Interacting Protein) Regulates Ischemia-Induced Microthrombosis Through Integrin αIIbβ3-Mediated Outside-In Signaling and Hypoxia Responses in Platelets.</ArticleTitle>
<Pagination><MedlinePgn>2793-2805</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1161/ATVBAHA.118.311822</ELocationID>
<Abstract><AbstractText>Objective- Microthrombosis as a serious consequence of myocardial infarction, impairs the microvascular environment and increases the occurrences of heart failure, arrhythmia, and death. Sin1 (stress-activated protein kinase-interacting protein) as an essential component of mTORC2 (mammalian target of rapamycin complex 2) is required for cell proliferation and metabolism in response to nutrients, stress, and reactive oxygen species and activates Akt and PKC (protein kinase C). However, the activation and function of Sin1/mTORC2 in ischemia-induced microthrombosis remain poorly understood. Approach and Results- The phosphorylation of the mTORC2 target Akt at S473 (serine 473) was significantly elevated in platelets from the distal end of left anterior descending obstructions from patients who underwent off-pump coronary artery bypass grafting compared with platelets from healthy subjects. Consistent with this finding, phosphorylation of T86 in Sin1 was also dramatically increased. Importantly, the augmented levels of phosphorylated Sin1 and Akt in platelets from 61 preoperative patients with ST-segment-elevation myocardial infarction correlated well with the no-reflow phenomena observed after revascularization. Platelet-specific Sin1 deficiency mice and Sin1 T86 phosphorylation deficiency mice were established to explore the underlying mechanisms in platelet activation. Mechanistically, Sin1 T86 phosphorylation amplifies mTORC2-mediated downstream signals; it is also required for αIIbβ3-mediated outside-in signaling and plays a role in generating hypoxia/reactive oxygen species through NAD<sup>+</sup>
/Sirt3 (sirtuin 3)/SOD2 (superoxide dismutase 2) pathway. Importantly, Sin1 deletion in platelets protected mice from ischemia-induced microvascular embolization and subsequent heart dysfunction in a mouse model of myocardial infarction. Conclusions- Together, the results of our study reveal a novel role for Sin1 in platelet activation. Thus, Sin1 may be a valuable therapeutic target for interventions for ischemia-induced myocardial infarction deterioration.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Yanyan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ouyang</LastName>
<ForeName>Xinxing</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yan</LastName>
<ForeName>Lichong</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Mingliang</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology, Shanghai Jiao Tong University School of Medicine Affiliated Ninth People's Hospital, Shanghai, China (M.Z., Z.H.).</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hu</LastName>
<ForeName>Zhenlei</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology, Shanghai Jiao Tong University School of Medicine Affiliated Ninth People's Hospital, Shanghai, China (M.Z., Z.H.).</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gu</LastName>
<ForeName>Jianmin</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Cardiovascular Surgery, Renji Hospital (J.G., S.X.), Shanghai Jiao Tong University School of Medicine, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fan</LastName>
<ForeName>Xuemei</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Lin</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Junfeng</ForeName>
<Initials>J</Initials>
</Author>
<Author ValidYN="Y"><LastName>Xue</LastName>
<ForeName>Song</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Cardiovascular Surgery, Renji Hospital (J.G., S.X.), Shanghai Jiao Tong University School of Medicine, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Guoqiang</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology (G.C.), Shanghai Jiao Tong University School of Medicine, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Su</LastName>
<ForeName>Bing</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology and Molecular Cell Biology (X.O., L.Y., B.S.), Shanghai Jiao Tong University School of Medicine, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Junling</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>From the Department of Biochemistry and Molecular Cell Biology (Y.X., X.F., L.Z., J.L.), Shanghai Jiao Tong University School of Medicine, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Collaborative Innovation Center of Hematology, Soochow University, China (J.L.).</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
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<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Arterioscler Thromb Vasc Biol</MedlineTA>
<NlmUniqueID>9505803</NlmUniqueID>
<ISSNLinking>1079-5642</ISSNLinking>
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<NameOfSubstance UI="D048868">Adaptor Proteins, Signal Transducing</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance>
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<NameOfSubstance UI="C493277">MAPKAP1 protein, human</NameOfSubstance>
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<Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber>
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<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
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<Chemical><RegistryNumber>EC 3.5.1.-</RegistryNumber>
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<QualifierName UI="Q000097" MajorTopicYN="Y">blood</QualifierName>
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<MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName>
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<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001792" MajorTopicYN="N">Blood Platelets</DescriptorName>
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</MeshHeading>
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<QualifierName UI="Q000097" MajorTopicYN="Y">blood</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015687" MajorTopicYN="N">Cell Hypoxia</DescriptorName>
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<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
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<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
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<MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName>
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<QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName>
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<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D056566" MajorTopicYN="N">Sirtuin 3</DescriptorName>
<QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName>
<QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
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<QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName>
<QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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</MeshHeadingList>
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<Keyword MajorTopicYN="Y">hypoxia</Keyword>
<Keyword MajorTopicYN="Y">myocardial infarction</Keyword>
<Keyword MajorTopicYN="Y">protein kinase C</Keyword>
<Keyword MajorTopicYN="Y">serine</Keyword>
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<Month>12</Month>
<Day>21</Day>
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<name sortKey="Zhang, Mingliang" sort="Zhang, Mingliang" uniqKey="Zhang M" first="Mingliang" last="Zhang">Mingliang Zhang</name>
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<country name="République populaire de Chine"><noRegion><name sortKey="Xu, Yanyan" sort="Xu, Yanyan" uniqKey="Xu Y" first="Yanyan" last="Xu">Yanyan Xu</name>
</noRegion>
<name sortKey="Chen, Guoqiang" sort="Chen, Guoqiang" uniqKey="Chen G" first="Guoqiang" last="Chen">Guoqiang Chen</name>
<name sortKey="Fan, Xuemei" sort="Fan, Xuemei" uniqKey="Fan X" first="Xuemei" last="Fan">Xuemei Fan</name>
<name sortKey="Gu, Jianmin" sort="Gu, Jianmin" uniqKey="Gu J" first="Jianmin" last="Gu">Jianmin Gu</name>
<name sortKey="Liu, Junling" sort="Liu, Junling" uniqKey="Liu J" first="Junling" last="Liu">Junling Liu</name>
<name sortKey="Ouyang, Xinxing" sort="Ouyang, Xinxing" uniqKey="Ouyang X" first="Xinxing" last="Ouyang">Xinxing Ouyang</name>
<name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name>
<name sortKey="Xue, Song" sort="Xue, Song" uniqKey="Xue S" first="Song" last="Xue">Song Xue</name>
<name sortKey="Yan, Lichong" sort="Yan, Lichong" uniqKey="Yan L" first="Lichong" last="Yan">Lichong Yan</name>
<name sortKey="Zhang, Lin" sort="Zhang, Lin" uniqKey="Zhang L" first="Lin" last="Zhang">Lin Zhang</name>
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Serveur d'exploration sur la rapamycine et les champignons

Sin1 (Stress-Activated Protein Kinase-Interacting Protein) Regulates Ischemia-Induced Microthrombosis Through Integrin αIIbβ3-Mediated Outside-In Signaling and Hypoxia Responses in Platelets.

Sin1 (Stress-Activated Protein Kinase-Interacting Protein) Regulates Ischemia-Induced Microthrombosis Through Integrin αIIbβ3-Mediated Outside-In Signaling and Hypoxia Responses in Platelets.

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