Exosomes derived from cardiac progenitor cells attenuate CVB3-induced apoptosis via abrogating the proliferation of CVB3 and modulating the mTOR signaling pathways.
Identifieur interne : 000343 ( Main/Exploration ); précédent : 000342; suivant : 000344Exosomes derived from cardiac progenitor cells attenuate CVB3-induced apoptosis via abrogating the proliferation of CVB3 and modulating the mTOR signaling pathways.
Auteurs : Xin Li [République populaire de Chine] ; Zuocheng Yang [République populaire de Chine] ; Wenyuan Nie [République populaire de Chine] ; Jie Jiang [République populaire de Chine] ; Shentang Li [République populaire de Chine] ; Zhuoying Li [République populaire de Chine] ; Lang Tian [République populaire de Chine] ; Xing Ma [République populaire de Chine]Source :
- Cell death & disease [ 2041-4889 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Apoptose (physiologie), Cellules souches (cytologie), Cellules souches (métabolisme), Entérovirus humain B (physiologie), Exosomes (métabolisme), Infections à virus coxsackie (anatomopathologie), Infections à virus coxsackie (métabolisme), Infections à virus coxsackie (thérapie), Infections à virus coxsackie (virologie), Lignée cellulaire (MeSH), Myocarde (cytologie), Myocarde (métabolisme), Myocardite (anatomopathologie), Myocardite (métabolisme), Myocardite (thérapie), Myocardite (virologie), Mâle (MeSH), Prolifération cellulaire (physiologie), Rat Sprague-Dawley (MeSH), Rats (MeSH), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH).
- MESH :
- anatomopathologie : Infections à virus coxsackie, Myocardite.
- cytologie : Cellules souches, Myocarde.
- métabolisme : Cellules souches, Exosomes, Infections à virus coxsackie, Myocarde, Myocardite, Sérine-thréonine kinases TOR.
- physiologie : Apoptose, Entérovirus humain B, Prolifération cellulaire.
- thérapie : Infections à virus coxsackie, Myocardite.
- virologie : Infections à virus coxsackie, Myocardite.
- Animaux, Lignée cellulaire, Mâle, Rat Sprague-Dawley, Rats, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Apoptosis (physiology), Cell Line (MeSH), Cell Proliferation (physiology), Coxsackievirus Infections (metabolism), Coxsackievirus Infections (pathology), Coxsackievirus Infections (therapy), Coxsackievirus Infections (virology), Enterovirus B, Human (physiology), Exosomes (metabolism), Male (MeSH), Myocarditis (metabolism), Myocarditis (pathology), Myocarditis (therapy), Myocarditis (virology), Myocardium (cytology), Myocardium (metabolism), Rats (MeSH), Rats, Sprague-Dawley (MeSH), Signal Transduction (MeSH), Stem Cells (cytology), Stem Cells (metabolism), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , metabolism : TOR Serine-Threonine Kinases.
- cytology : Myocardium, Stem Cells.
- metabolism : Coxsackievirus Infections, Exosomes, Myocarditis, Myocardium, Stem Cells.
- pathology : Coxsackievirus Infections, Myocarditis.
- physiology : Apoptosis, Cell Proliferation, Enterovirus B, Human.
- therapy : Coxsackievirus Infections, Myocarditis.
- virology : Coxsackievirus Infections, Myocarditis.
- Animals, Cell Line, Male, Rats, Rats, Sprague-Dawley, Signal Transduction.
Abstract
Viral myocarditis is potentially fatal and lacking a specific treatment. Exosomes secreted by cardiac progenitor cells (CPCs) have emerged as a promising tool for cardioprotection and repair. In this study, we investigated whether CPCs-derived exosomes (CPCs-Ex) could utilize the mTOR signal pathway to reduce the apoptosis in viral myocarditis. In vitro, exosomes were, respectively, added to H9C2 cells after CVB3 infection to detect the anti-apoptosis effect of CPCs-Ex. Compared with the controls, the apoptosis rate was reduced, accompanied with the depressed expression of viral capsid protein 1 (VP1) and pro-apoptosis factors of Bim/caspase families. Meanwhile, the phosphorylation of Akt, mTOR, and p70S6K were promoted, but that of 4EBP1 was suppressed. In vivo, the results of apoptosis, expression of CVB3 and pro-apoptosis factors, and phosphorylation of Akt/mTOR factors of CVB3-infected cardiomyocytes were consistent with that of vitro. Following that, we use Rapamycin and MK-2206 to inhibit the Akt/mTOR signaling pathway, meanwhile, Rattus 4EBP1, p70S6K, Akt1 and Akt2 were transfected to H9C2 cells to establish the stably transfected cell lines. In the group with Rapamycin or MK-2206 pretreatment, CPCs-Ex also could decrease the apoptosis of H9C2 cells and expression of CVB3 mRNA, followed by decreased expression of apoptosis factors. In Akt2, p70S6K and 4EBP1 overexpression groups, CPCs-Ex promoted CVB3-induced apoptosis, VP1 expression and cleavage of caspase-3. Our results therefore identify CPCs-Ex exerts an anti-apoptosis effect in CVB3-infected cells by abrogating the proliferation of CVB3 and modulating the mTOR signaling pathways as well as the expression of Bcl-2 and caspase families. Viral myocarditis, mainly caused by CVB3 infection, is lacking a specific treatment. Our study identified an anti-apoptosis role of CPCs-Ex in CVB3-infected cells and rats, which shown that CPCs-Ex may be an effective tool to treat viral myocarditis. We believe that with more in-depth research on the functionality of CPCs-Ex, there will be a breakthrough in the treatment of viral myocarditis.
DOI: 10.1038/s41419-019-1910-9
PubMed: 31534118
PubMed Central: PMC6751166
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Apoptosis (physiology)</term>
<term>Cell Line (MeSH)</term>
<term>Cell Proliferation (physiology)</term>
<term>Coxsackievirus Infections (metabolism)</term>
<term>Coxsackievirus Infections (pathology)</term>
<term>Coxsackievirus Infections (therapy)</term>
<term>Coxsackievirus Infections (virology)</term>
<term>Enterovirus B, Human (physiology)</term>
<term>Exosomes (metabolism)</term>
<term>Male (MeSH)</term>
<term>Myocarditis (metabolism)</term>
<term>Myocarditis (pathology)</term>
<term>Myocarditis (therapy)</term>
<term>Myocarditis (virology)</term>
<term>Myocardium (cytology)</term>
<term>Myocardium (metabolism)</term>
<term>Rats (MeSH)</term>
<term>Rats, Sprague-Dawley (MeSH)</term>
<term>Signal Transduction (MeSH)</term>
<term>Stem Cells (cytology)</term>
<term>Stem Cells (metabolism)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
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<term>Apoptose (physiologie)</term>
<term>Cellules souches (cytologie)</term>
<term>Cellules souches (métabolisme)</term>
<term>Entérovirus humain B (physiologie)</term>
<term>Exosomes (métabolisme)</term>
<term>Infections à virus coxsackie (anatomopathologie)</term>
<term>Infections à virus coxsackie (métabolisme)</term>
<term>Infections à virus coxsackie (thérapie)</term>
<term>Infections à virus coxsackie (virologie)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Myocarde (cytologie)</term>
<term>Myocarde (métabolisme)</term>
<term>Myocardite (anatomopathologie)</term>
<term>Myocardite (métabolisme)</term>
<term>Myocardite (thérapie)</term>
<term>Myocardite (virologie)</term>
<term>Mâle (MeSH)</term>
<term>Prolifération cellulaire (physiologie)</term>
<term>Rat Sprague-Dawley (MeSH)</term>
<term>Rats (MeSH)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Transduction du signal (MeSH)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Infections à virus coxsackie</term>
<term>Myocardite</term>
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<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules souches</term>
<term>Myocarde</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Myocardium</term>
<term>Stem Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Coxsackievirus Infections</term>
<term>Exosomes</term>
<term>Myocarditis</term>
<term>Myocardium</term>
<term>Stem Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules souches</term>
<term>Exosomes</term>
<term>Infections à virus coxsackie</term>
<term>Myocarde</term>
<term>Myocardite</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Coxsackievirus Infections</term>
<term>Myocarditis</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term>
<term>Entérovirus humain B</term>
<term>Prolifération cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term>
<term>Cell Proliferation</term>
<term>Enterovirus B, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Coxsackievirus Infections</term>
<term>Myocarditis</term>
</keywords>
<keywords scheme="MESH" qualifier="thérapie" xml:lang="fr"><term>Infections à virus coxsackie</term>
<term>Myocardite</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à virus coxsackie</term>
<term>Myocardite</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Coxsackievirus Infections</term>
<term>Myocarditis</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line</term>
<term>Male</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Lignée cellulaire</term>
<term>Mâle</term>
<term>Rat Sprague-Dawley</term>
<term>Rats</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">Viral myocarditis is potentially fatal and lacking a specific treatment. Exosomes secreted by cardiac progenitor cells (CPCs) have emerged as a promising tool for cardioprotection and repair. In this study, we investigated whether CPCs-derived exosomes (CPCs-Ex) could utilize the mTOR signal pathway to reduce the apoptosis in viral myocarditis. In vitro, exosomes were, respectively, added to H9C2 cells after CVB3 infection to detect the anti-apoptosis effect of CPCs-Ex. Compared with the controls, the apoptosis rate was reduced, accompanied with the depressed expression of viral capsid protein 1 (VP1) and pro-apoptosis factors of Bim/caspase families. Meanwhile, the phosphorylation of Akt, mTOR, and p70S6K were promoted, but that of 4EBP1 was suppressed. In vivo, the results of apoptosis, expression of CVB3 and pro-apoptosis factors, and phosphorylation of Akt/mTOR factors of CVB3-infected cardiomyocytes were consistent with that of vitro. Following that, we use Rapamycin and MK-2206 to inhibit the Akt/mTOR signaling pathway, meanwhile, Rattus 4EBP1, p70S6K, Akt1 and Akt2 were transfected to H9C2 cells to establish the stably transfected cell lines. In the group with Rapamycin or MK-2206 pretreatment, CPCs-Ex also could decrease the apoptosis of H9C2 cells and expression of CVB3 mRNA, followed by decreased expression of apoptosis factors. In Akt2, p70S6K and 4EBP1 overexpression groups, CPCs-Ex promoted CVB3-induced apoptosis, VP1 expression and cleavage of caspase-3. Our results therefore identify CPCs-Ex exerts an anti-apoptosis effect in CVB3-infected cells by abrogating the proliferation of CVB3 and modulating the mTOR signaling pathways as well as the expression of Bcl-2 and caspase families. Viral myocarditis, mainly caused by CVB3 infection, is lacking a specific treatment. Our study identified an anti-apoptosis role of CPCs-Ex in CVB3-infected cells and rats, which shown that CPCs-Ex may be an effective tool to treat viral myocarditis. We believe that with more in-depth research on the functionality of CPCs-Ex, there will be a breakthrough in the treatment of viral myocarditis.</div>
</front>
</TEI>
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<DateCompleted><Year>2020</Year>
<Month>09</Month>
<Day>23</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>09</Month>
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<Month>09</Month>
<Day>18</Day>
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<Title>Cell death & disease</Title>
<ISOAbbreviation>Cell Death Dis</ISOAbbreviation>
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<ArticleTitle>Exosomes derived from cardiac progenitor cells attenuate CVB3-induced apoptosis via abrogating the proliferation of CVB3 and modulating the mTOR signaling pathways.</ArticleTitle>
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<Abstract><AbstractText>Viral myocarditis is potentially fatal and lacking a specific treatment. Exosomes secreted by cardiac progenitor cells (CPCs) have emerged as a promising tool for cardioprotection and repair. In this study, we investigated whether CPCs-derived exosomes (CPCs-Ex) could utilize the mTOR signal pathway to reduce the apoptosis in viral myocarditis. In vitro, exosomes were, respectively, added to H9C2 cells after CVB3 infection to detect the anti-apoptosis effect of CPCs-Ex. Compared with the controls, the apoptosis rate was reduced, accompanied with the depressed expression of viral capsid protein 1 (VP1) and pro-apoptosis factors of Bim/caspase families. Meanwhile, the phosphorylation of Akt, mTOR, and p70S6K were promoted, but that of 4EBP1 was suppressed. In vivo, the results of apoptosis, expression of CVB3 and pro-apoptosis factors, and phosphorylation of Akt/mTOR factors of CVB3-infected cardiomyocytes were consistent with that of vitro. Following that, we use Rapamycin and MK-2206 to inhibit the Akt/mTOR signaling pathway, meanwhile, Rattus 4EBP1, p70S6K, Akt1 and Akt2 were transfected to H9C2 cells to establish the stably transfected cell lines. In the group with Rapamycin or MK-2206 pretreatment, CPCs-Ex also could decrease the apoptosis of H9C2 cells and expression of CVB3 mRNA, followed by decreased expression of apoptosis factors. In Akt2, p70S6K and 4EBP1 overexpression groups, CPCs-Ex promoted CVB3-induced apoptosis, VP1 expression and cleavage of caspase-3. Our results therefore identify CPCs-Ex exerts an anti-apoptosis effect in CVB3-infected cells by abrogating the proliferation of CVB3 and modulating the mTOR signaling pathways as well as the expression of Bcl-2 and caspase families. Viral myocarditis, mainly caused by CVB3 infection, is lacking a specific treatment. Our study identified an anti-apoptosis role of CPCs-Ex in CVB3-infected cells and rats, which shown that CPCs-Ex may be an effective tool to treat viral myocarditis. We believe that with more in-depth research on the functionality of CPCs-Ex, there will be a breakthrough in the treatment of viral myocarditis.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Xin</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, the Third Xiangya Hospital, Central South University, Changsha, China. joyeelee@csu.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Zuocheng</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, the Third Xiangya Hospital, Central South University, Changsha, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nie</LastName>
<ForeName>Wenyuan</ForeName>
<Initials>W</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-6532-7237</Identifier>
<AffiliationInfo><Affiliation>Department of Urology, Chinese People's Liberation Army, 89th Hospital, Weifang, Shandong, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jiang</LastName>
<ForeName>Jie</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, the Third Xiangya Hospital, Central South University, Changsha, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Shentang</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, the Third Xiangya Hospital, Central South University, Changsha, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Zhuoying</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, the Third Xiangya Hospital, Central South University, Changsha, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tian</LastName>
<ForeName>Lang</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, the Third Xiangya Hospital, Central South University, Changsha, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ma</LastName>
<ForeName>Xing</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Sate Key Laboratory of Advanced Welding and Joining, Harbin Institute of Technology (Shenzhen), Shenzhen, China.</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>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>09</Month>
<Day>18</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Cell Death Dis</MedlineTA>
<NlmUniqueID>101524092</NlmUniqueID>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="C546845">mTOR protein, rat</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003384" MajorTopicYN="N">Coxsackievirus Infections</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D029822" MajorTopicYN="N">Enterovirus B, Human</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D055354" MajorTopicYN="N">Exosomes</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009205" MajorTopicYN="N">Myocarditis</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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<MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013234" MajorTopicYN="N">Stem Cells</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
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<Month>04</Month>
<Day>16</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
<Month>08</Month>
<Day>26</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2019</Year>
<Month>08</Month>
<Day>18</Day>
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<PubMedPubDate PubStatus="entrez"><Year>2019</Year>
<Month>9</Month>
<Day>20</Day>
<Hour>6</Hour>
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<Month>9</Month>
<Day>20</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="medline"><Year>2020</Year>
<Month>9</Month>
<Day>24</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PublicationStatus>epublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">31534118</ArticleId>
<ArticleId IdType="doi">10.1038/s41419-019-1910-9</ArticleId>
<ArticleId IdType="pii">10.1038/s41419-019-1910-9</ArticleId>
<ArticleId IdType="pmc">PMC6751166</ArticleId>
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<affiliations><list><country><li>République populaire de Chine</li>
</country>
<region><li>Guangdong</li>
</region>
<settlement><li>Shenzhen</li>
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<tree><country name="République populaire de Chine"><noRegion><name sortKey="Li, Xin" sort="Li, Xin" uniqKey="Li X" first="Xin" last="Li">Xin Li</name>
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<name sortKey="Jiang, Jie" sort="Jiang, Jie" uniqKey="Jiang J" first="Jie" last="Jiang">Jie Jiang</name>
<name sortKey="Li, Shentang" sort="Li, Shentang" uniqKey="Li S" first="Shentang" last="Li">Shentang Li</name>
<name sortKey="Li, Zhuoying" sort="Li, Zhuoying" uniqKey="Li Z" first="Zhuoying" last="Li">Zhuoying Li</name>
<name sortKey="Ma, Xing" sort="Ma, Xing" uniqKey="Ma X" first="Xing" last="Ma">Xing Ma</name>
<name sortKey="Nie, Wenyuan" sort="Nie, Wenyuan" uniqKey="Nie W" first="Wenyuan" last="Nie">Wenyuan Nie</name>
<name sortKey="Tian, Lang" sort="Tian, Lang" uniqKey="Tian L" first="Lang" last="Tian">Lang Tian</name>
<name sortKey="Yang, Zuocheng" sort="Yang, Zuocheng" uniqKey="Yang Z" first="Zuocheng" last="Yang">Zuocheng Yang</name>
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