CovidSeniorV1, Main, Exploration, bibRecord, 000249

SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19.

Identifieur interne : 000249 ( Main/Exploration ); précédent : 000248; suivant : 000250

SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19.

Source :

Journal of hematology & oncology [ 1756-8722 ] ; 2020.

RBID : pubmed:32887634

Descripteurs français

English descriptors

KwdEn :
- Adult (MeSH), Aged (MeSH), Animals (MeSH), Betacoronavirus (genetics), Betacoronavirus (metabolism), Blood Platelets (metabolism), Caco-2 Cells (MeSH), Coronavirus Infections (metabolism), Coronavirus Infections (virology), Female (MeSH), HeLa Cells (MeSH), Humans (MeSH), Male (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mice, Transgenic (MeSH), Middle Aged (MeSH), PC-3 Cells (MeSH), Pandemics (MeSH), Peptidyl-Dipeptidase A (genetics), Peptidyl-Dipeptidase A (metabolism), Platelet Aggregation (immunology), Platelet Count (MeSH), Pneumonia, Viral (metabolism), Pneumonia, Viral (virology), RNA, Viral (blood), Serine Endopeptidases (metabolism), Spike Glycoprotein, Coronavirus (metabolism), Thrombosis (metabolism), Thrombosis (virology).
MESH :
- chemical , blood : RNA, Viral.
- chemical , genetics : Peptidyl-Dipeptidase A.
- genetics : Betacoronavirus.
- immunology : Platelet Aggregation.
- metabolism : Betacoronavirus, Blood Platelets, Coronavirus Infections, Peptidyl-Dipeptidase A, Pneumonia, Viral, Serine Endopeptidases, Spike Glycoprotein, Coronavirus, Thrombosis.
- virology : Coronavirus Infections, Pneumonia, Viral, Thrombosis.
- Adult, Aged, Animals, Caco-2 Cells, Female, HeLa Cells, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Middle Aged, PC-3 Cells, Pandemics, Platelet Count.

Abstract

BACKGROUND

Critically ill patients diagnosed with COVID-19 may develop a pro-thrombotic state that places them at a dramatically increased lethal risk. Although platelet activation is critical for thrombosis and is responsible for the thrombotic events and cardiovascular complications, the role of platelets in the pathogenesis of COVID-19 remains unclear.

METHODS

Using platelets from healthy volunteers, non-COVID-19 and COVID-19 patients, as well as wild-type and hACE2 transgenic mice, we evaluated the changes in platelet and coagulation parameters in COVID-19 patients. We investigated ACE2 expression and direct effect of SARS-CoV-2 virus on platelets by RT-PCR, flow cytometry, Western blot, immunofluorescence, and platelet functional studies in vitro, FeCl

RESULTS

We demonstrated that COVID-19 patients present with increased mean platelet volume (MPV) and platelet hyperactivity, which correlated with a decrease in overall platelet count. Detectable SARS-CoV-2 RNA in the blood stream was associated with platelet hyperactivity in critically ill patients. Platelets expressed ACE2, a host cell receptor for SARS-CoV-2, and TMPRSS2, a serine protease for Spike protein priming. SARS-CoV-2 and its Spike protein directly enhanced platelet activation such as platelet aggregation, PAC-1 binding, CD62P expression, α granule secretion, dense granule release, platelet spreading, and clot retraction in vitro, and thereby Spike protein enhanced thrombosis formation in wild-type mice transfused with hACE2 transgenic platelets, but this was not observed in animals transfused with wild-type platelets in vivo. Further, we provided evidence suggesting that the MAPK pathway, downstream of ACE2, mediates the potentiating role of SARS-CoV-2 on platelet activation, and that platelet ACE2 expression decreases following SARS-COV-2 stimulation. SARS-CoV-2 and its Spike protein directly stimulated platelets to facilitate the release of coagulation factors, the secretion of inflammatory factors, and the formation of leukocyte-platelet aggregates. Recombinant human ACE2 protein and anti-Spike monoclonal antibody could inhibit SARS-CoV-2 Spike protein-induced platelet activation.

CONCLUSIONS

Our findings uncovered a novel function of SARS-CoV-2 on platelet activation via binding of Spike to ACE2. SARS-CoV-2-induced platelet activation may participate in thrombus formation and inflammatory responses in COVID-19 patients.

DOI: 10.1186/s13045-020-00954-7
PubMed: 32887634
PubMed Central: PMC7471641

Affiliations:

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Le document en format XML

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<author><name sortKey="Dong, Jianzeng" sort="Dong, Jianzeng" uniqKey="Dong J" first="Jianzeng" last="Dong">Jianzeng Dong</name>
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<author><name sortKey="Yuan, Zhenghong" sort="Yuan, Zhenghong" uniqKey="Yuan Z" first="Zhenghong" last="Yuan">Zhenghong Yuan</name>
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<author><name sortKey="Zhang, Yi" sort="Zhang, Yi" uniqKey="Zhang Y" first="Yi" last="Zhang">Yi Zhang</name>
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<author><name sortKey="Hu, Liang" sort="Hu, Liang" uniqKey="Hu L" first="Liang" last="Hu">Liang Hu</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19.</title>
<author><name sortKey="Zhang, Si" sort="Zhang, Si" uniqKey="Zhang S" first="Si" last="Zhang">Si Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, NHC Key Laboratory of Glycoconjugates Research, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China. zhangsi@fudan.edu.cn.</nlm:affiliation>
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</affiliation>
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<author><name sortKey="Liu, Yangyang" sort="Liu, Yangyang" uniqKey="Liu Y" first="Yangyang" last="Liu">Yangyang Liu</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Wang, Xiaofang" sort="Wang, Xiaofang" uniqKey="Wang X" first="Xiaofang" last="Wang">Xiaofang Wang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
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<wicri:noRegion>450052</wicri:noRegion>
</affiliation>
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<author><name sortKey="Yang, Li" sort="Yang, Li" uniqKey="Yang L" first="Li" last="Yang">Li Yang</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Li, Haishan" sort="Li, Haishan" uniqKey="Li H" first="Haishan" last="Li">Haishan Li</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Emergency, Affiliated Hospital of Anhui Medical University, Hefei, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Emergency, Affiliated Hospital of Anhui Medical University, Hefei</wicri:regionArea>
<placeName><settlement type="city">Hefei</settlement>
<region type="province">Anhui</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Wang, Yuyan" sort="Wang, Yuyan" uniqKey="Wang Y" first="Yuyan" last="Wang">Yuyan Wang</name>
<affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), and Department of Medical Microbiology and Parasitology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.</nlm:affiliation>
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</affiliation>
</author>
<author><name sortKey="Liu, Mengduan" sort="Liu, Mengduan" uniqKey="Liu M" first="Mengduan" last="Liu">Mengduan Liu</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052</wicri:regionArea>
<wicri:noRegion>450052</wicri:noRegion>
</affiliation>
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<author><name sortKey="Zhao, Xiaoyan" sort="Zhao, Xiaoyan" uniqKey="Zhao X" first="Xiaoyan" last="Zhao">Xiaoyan Zhao</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052</wicri:regionArea>
<wicri:noRegion>450052</wicri:noRegion>
</affiliation>
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<author><name sortKey="Xie, Youhua" sort="Xie, Youhua" uniqKey="Xie Y" first="Youhua" last="Xie">Youhua Xie</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Yang, Yan" sort="Yang, Yan" uniqKey="Yang Y" first="Yan" last="Yang">Yan Yang</name>
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<author><name sortKey="Zhang, Shenghui" sort="Zhang, Shenghui" uniqKey="Zhang S" first="Shenghui" last="Zhang">Shenghui Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Hematology, Wenzhou Key Laboratory of Hematology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Hematology, Wenzhou Key Laboratory of Hematology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou</wicri:regionArea>
<wicri:noRegion>Wenzhou</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Fan, Zhichao" sort="Fan, Zhichao" uniqKey="Fan Z" first="Zhichao" last="Fan">Zhichao Fan</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, School of Medicine, UConn Health, Farmington, CT, 06030, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Immunology, School of Medicine, UConn Health, Farmington, CT, 06030</wicri:regionArea>
<wicri:noRegion>06030</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Dong, Jianzeng" sort="Dong, Jianzeng" uniqKey="Dong J" first="Jianzeng" last="Dong">Jianzeng Dong</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052</wicri:regionArea>
<wicri:noRegion>450052</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Yuan, Zhenghong" sort="Yuan, Zhenghong" uniqKey="Yuan Z" first="Zhenghong" last="Yuan">Zhenghong Yuan</name>
<affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), and Department of Medical Microbiology and Parasitology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), and Department of Medical Microbiology and Parasitology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai</wicri:regionArea>
<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Ding, Zhongren" sort="Ding, Zhongren" uniqKey="Ding Z" first="Zhongren" last="Ding">Zhongren Ding</name>
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<country xml:lang="fr">République populaire de Chine</country>
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</affiliation>
</author>
<author><name sortKey="Zhang, Yi" sort="Zhang, Yi" uniqKey="Zhang Y" first="Yi" last="Zhang">Yi Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>Biotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. yizhang@zzu.edu.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Biotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052</wicri:regionArea>
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</affiliation>
</author>
<author><name sortKey="Hu, Liang" sort="Hu, Liang" uniqKey="Hu L" first="Liang" last="Hu">Liang Hu</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China. fcchul@zzu.edu.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
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<series><title level="j">Journal of hematology & oncology</title>
<idno type="eISSN">1756-8722</idno>
<imprint><date when="2020" type="published">2020</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult (MeSH)</term>
<term>Aged (MeSH)</term>
<term>Animals (MeSH)</term>
<term>Betacoronavirus (genetics)</term>
<term>Betacoronavirus (metabolism)</term>
<term>Blood Platelets (metabolism)</term>
<term>Caco-2 Cells (MeSH)</term>
<term>Coronavirus Infections (metabolism)</term>
<term>Coronavirus Infections (virology)</term>
<term>Female (MeSH)</term>
<term>HeLa Cells (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mice, Transgenic (MeSH)</term>
<term>Middle Aged (MeSH)</term>
<term>PC-3 Cells (MeSH)</term>
<term>Pandemics (MeSH)</term>
<term>Peptidyl-Dipeptidase A (genetics)</term>
<term>Peptidyl-Dipeptidase A (metabolism)</term>
<term>Platelet Aggregation (immunology)</term>
<term>Platelet Count (MeSH)</term>
<term>Pneumonia, Viral (metabolism)</term>
<term>Pneumonia, Viral (virology)</term>
<term>RNA, Viral (blood)</term>
<term>Serine Endopeptidases (metabolism)</term>
<term>Spike Glycoprotein, Coronavirus (metabolism)</term>
<term>Thrombosis (metabolism)</term>
<term>Thrombosis (virology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ARN viral (sang)</term>
<term>Adulte (MeSH)</term>
<term>Adulte d'âge moyen (MeSH)</term>
<term>Agrégation plaquettaire (immunologie)</term>
<term>Animaux (MeSH)</term>
<term>Betacoronavirus (génétique)</term>
<term>Betacoronavirus (métabolisme)</term>
<term>Cellules Caco-2 (MeSH)</term>
<term>Cellules HeLa (MeSH)</term>
<term>Cellules PC-3 (MeSH)</term>
<term>Femelle (MeSH)</term>
<term>Glycoprotéine de spicule des coronavirus (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Infections à coronavirus (métabolisme)</term>
<term>Infections à coronavirus (virologie)</term>
<term>Mâle (MeSH)</term>
<term>Numération des plaquettes (MeSH)</term>
<term>Pandémies (MeSH)</term>
<term>Peptidyl-Dipeptidase A (génétique)</term>
<term>Peptidyl-Dipeptidase A (métabolisme)</term>
<term>Plaquettes (métabolisme)</term>
<term>Pneumopathie virale (métabolisme)</term>
<term>Pneumopathie virale (virologie)</term>
<term>Serine endopeptidases (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Souris transgéniques (MeSH)</term>
<term>Sujet âgé (MeSH)</term>
<term>Thrombose (métabolisme)</term>
<term>Thrombose (virologie)</term>
</keywords>
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Peptidyl-Dipeptidase A</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Betacoronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Betacoronavirus</term>
<term>Peptidyl-Dipeptidase A</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Agrégation plaquettaire</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Platelet Aggregation</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Betacoronavirus</term>
<term>Blood Platelets</term>
<term>Coronavirus Infections</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Pneumonia, Viral</term>
<term>Serine Endopeptidases</term>
<term>Spike Glycoprotein, Coronavirus</term>
<term>Thrombosis</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Betacoronavirus</term>
<term>Glycoprotéine de spicule des coronavirus</term>
<term>Infections à coronavirus</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Plaquettes</term>
<term>Pneumopathie virale</term>
<term>Serine endopeptidases</term>
<term>Thrombose</term>
</keywords>
<keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>ARN viral</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Pneumopathie virale</term>
<term>Thrombose</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Coronavirus Infections</term>
<term>Pneumonia, Viral</term>
<term>Thrombosis</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Animals</term>
<term>Caco-2 Cells</term>
<term>Female</term>
<term>HeLa Cells</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Transgenic</term>
<term>Middle Aged</term>
<term>PC-3 Cells</term>
<term>Pandemics</term>
<term>Platelet Count</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Adulte</term>
<term>Adulte d'âge moyen</term>
<term>Animaux</term>
<term>Cellules Caco-2</term>
<term>Cellules HeLa</term>
<term>Cellules PC-3</term>
<term>Femelle</term>
<term>Humains</term>
<term>Mâle</term>
<term>Numération des plaquettes</term>
<term>Pandémies</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
<term>Sujet âgé</term>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>Critically ill patients diagnosed with COVID-19 may develop a pro-thrombotic state that places them at a dramatically increased lethal risk. Although platelet activation is critical for thrombosis and is responsible for the thrombotic events and cardiovascular complications, the role of platelets in the pathogenesis of COVID-19 remains unclear.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>Using platelets from healthy volunteers, non-COVID-19 and COVID-19 patients, as well as wild-type and hACE2 transgenic mice, we evaluated the changes in platelet and coagulation parameters in COVID-19 patients. We investigated ACE2 expression and direct effect of SARS-CoV-2 virus on platelets by RT-PCR, flow cytometry, Western blot, immunofluorescence, and platelet functional studies in vitro, FeCl</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>We demonstrated that COVID-19 patients present with increased mean platelet volume (MPV) and platelet hyperactivity, which correlated with a decrease in overall platelet count. Detectable SARS-CoV-2 RNA in the blood stream was associated with platelet hyperactivity in critically ill patients. Platelets expressed ACE2, a host cell receptor for SARS-CoV-2, and TMPRSS2, a serine protease for Spike protein priming. SARS-CoV-2 and its Spike protein directly enhanced platelet activation such as platelet aggregation, PAC-1 binding, CD62P expression, α granule secretion, dense granule release, platelet spreading, and clot retraction in vitro, and thereby Spike protein enhanced thrombosis formation in wild-type mice transfused with hACE2 transgenic platelets, but this was not observed in animals transfused with wild-type platelets in vivo. Further, we provided evidence suggesting that the MAPK pathway, downstream of ACE2, mediates the potentiating role of SARS-CoV-2 on platelet activation, and that platelet ACE2 expression decreases following SARS-COV-2 stimulation. SARS-CoV-2 and its Spike protein directly stimulated platelets to facilitate the release of coagulation factors, the secretion of inflammatory factors, and the formation of leukocyte-platelet aggregates. Recombinant human ACE2 protein and anti-Spike monoclonal antibody could inhibit SARS-CoV-2 Spike protein-induced platelet activation.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>Our findings uncovered a novel function of SARS-CoV-2 on platelet activation via binding of Spike to ACE2. SARS-CoV-2-induced platelet activation may participate in thrombus formation and inflammatory responses in COVID-19 patients.</p>
</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32887634</PMID>
<DateCompleted><Year>2020</Year>
<Month>09</Month>
<Day>21</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>09</Month>
<Day>21</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1756-8722</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>13</Volume>
<Issue>1</Issue>
<PubDate><Year>2020</Year>
<Month>09</Month>
<Day>04</Day>
</PubDate>
</JournalIssue>
<Title>Journal of hematology & oncology</Title>
<ISOAbbreviation>J Hematol Oncol</ISOAbbreviation>
</Journal>
<ArticleTitle>SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19.</ArticleTitle>
<Pagination><MedlinePgn>120</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1186/s13045-020-00954-7</ELocationID>
<Abstract><AbstractText Label="BACKGROUND">Critically ill patients diagnosed with COVID-19 may develop a pro-thrombotic state that places them at a dramatically increased lethal risk. Although platelet activation is critical for thrombosis and is responsible for the thrombotic events and cardiovascular complications, the role of platelets in the pathogenesis of COVID-19 remains unclear.</AbstractText>
<AbstractText Label="METHODS">Using platelets from healthy volunteers, non-COVID-19 and COVID-19 patients, as well as wild-type and hACE2 transgenic mice, we evaluated the changes in platelet and coagulation parameters in COVID-19 patients. We investigated ACE2 expression and direct effect of SARS-CoV-2 virus on platelets by RT-PCR, flow cytometry, Western blot, immunofluorescence, and platelet functional studies in vitro, FeCl<sub>3</sub>
-induced thrombus formation in vivo, and thrombus formation under flow conditions ex vivo.</AbstractText>
<AbstractText Label="RESULTS">We demonstrated that COVID-19 patients present with increased mean platelet volume (MPV) and platelet hyperactivity, which correlated with a decrease in overall platelet count. Detectable SARS-CoV-2 RNA in the blood stream was associated with platelet hyperactivity in critically ill patients. Platelets expressed ACE2, a host cell receptor for SARS-CoV-2, and TMPRSS2, a serine protease for Spike protein priming. SARS-CoV-2 and its Spike protein directly enhanced platelet activation such as platelet aggregation, PAC-1 binding, CD62P expression, α granule secretion, dense granule release, platelet spreading, and clot retraction in vitro, and thereby Spike protein enhanced thrombosis formation in wild-type mice transfused with hACE2 transgenic platelets, but this was not observed in animals transfused with wild-type platelets in vivo. Further, we provided evidence suggesting that the MAPK pathway, downstream of ACE2, mediates the potentiating role of SARS-CoV-2 on platelet activation, and that platelet ACE2 expression decreases following SARS-COV-2 stimulation. SARS-CoV-2 and its Spike protein directly stimulated platelets to facilitate the release of coagulation factors, the secretion of inflammatory factors, and the formation of leukocyte-platelet aggregates. Recombinant human ACE2 protein and anti-Spike monoclonal antibody could inhibit SARS-CoV-2 Spike protein-induced platelet activation.</AbstractText>
<AbstractText Label="CONCLUSIONS">Our findings uncovered a novel function of SARS-CoV-2 on platelet activation via binding of Spike to ACE2. SARS-CoV-2-induced platelet activation may participate in thrombus formation and inflammatory responses in COVID-19 patients.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Si</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, NHC Key Laboratory of Glycoconjugates Research, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China. zhangsi@fudan.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Yangyang</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Xiaofang</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China.</Affiliation>
</AffiliationInfo>
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<ForeName>Li</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Biotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.</Affiliation>
</AffiliationInfo>
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<ForeName>Haishan</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Emergency, Affiliated Hospital of Anhui Medical University, Hefei, China.</Affiliation>
</AffiliationInfo>
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<ForeName>Yuyan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), and Department of Medical Microbiology and Parasitology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Mengduan</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China.</Affiliation>
</AffiliationInfo>
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<ForeName>Xiaoyan</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Xie</LastName>
<ForeName>Youhua</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), and Department of Medical Microbiology and Parasitology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Yan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>School of Public Health (Shenzhen), Sun Yat-sen University, Guangzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Shenghui</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Hematology, Wenzhou Key Laboratory of Hematology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fan</LastName>
<ForeName>Zhichao</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Immunology, School of Medicine, UConn Health, Farmington, CT, 06030, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dong</LastName>
<ForeName>Jianzeng</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yuan</LastName>
<ForeName>Zhenghong</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), and Department of Medical Microbiology and Parasitology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ding</LastName>
<ForeName>Zhongren</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Yi</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Biotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. yizhang@zzu.edu.cn.</Affiliation>
</AffiliationInfo>
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<AffiliationInfo><Affiliation>Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Cardiovascular Institute of Zhengzhou University, Zhengzhou, 450052, China. fcchul@zzu.edu.cn.</Affiliation>
</AffiliationInfo>
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<GrantList CompleteYN="Y"><Grant><GrantID>81803522</GrantID>
<Agency>Young Scientists Fund</Agency>
<Country>International</Country>
</Grant>
<Grant><GrantID>81900378</GrantID>
<Agency>Young Scientists Fund</Agency>
<Country>International</Country>
</Grant>
<Grant><GrantID>81970305</GrantID>
<Agency>National Natural Science Foundation of China (CN)</Agency>
<Country>International</Country>
</Grant>
<Grant><GrantID>81770137</GrantID>
<Agency>National Natural Science Foundation of China</Agency>
<Country>International</Country>
</Grant>
<Grant><GrantID>81573423</GrantID>
<Agency>National Natural Science Foundation of China</Agency>
<Country>International</Country>
</Grant>
<Grant><GrantID>81903603</GrantID>
<Agency>National Natural Science Foundation of China</Agency>
<Country>International</Country>
</Grant>
<Grant><GrantID>81400323</GrantID>
<Agency>National Natural Science Foundation of China</Agency>
<Country>International</Country>
</Grant>
<Grant><GrantID>201100310900</GrantID>
<Agency>Emergency Prevention and Control of COVID-19 Project of Henan Province</Agency>
<Country>International</Country>
</Grant>
<Grant><GrantID>2020M672292</GrantID>
<Agency>Postdoctoral Research Foundation of China</Agency>
<Country>International</Country>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
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<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
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<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
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SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19.

SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19.

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