Strain-stimulated hypertrophy in cardiac myocytes is mediated by reactive oxygen species-dependent Ras S-glutathiolation.
Identifieur interne : 000D12 ( Main/Exploration ); précédent : 000D11; suivant : 000D13Strain-stimulated hypertrophy in cardiac myocytes is mediated by reactive oxygen species-dependent Ras S-glutathiolation.
Auteurs : David R. Pimentel [États-Unis] ; Takeshi Adachi ; Yasuo Ido ; Tyler Heibeck ; Bingbing Jiang ; Yong Lee ; J Andres Melendez ; Richard A. Cohen ; Wilson S. ColucciSource :
- Journal of molecular and cellular cardiology [ 0022-2828 ] ; 2006.
Descripteurs français
- KwdFr :
- Adenoviridae (génétique), Animaux (MeSH), Animaux nouveau-nés (MeSH), Cardiomyopathie hypertrophique (métabolisme), Cardiomyopathie hypertrophique (étiologie), Catalase (génétique), Catalase (physiologie), Contrainte mécanique (MeSH), Cystéine (composition chimique), Espèces réactives de l'oxygène (MeSH), Extracellular Signal-Regulated MAP Kinases (biosynthèse), Extracellular Signal-Regulated MAP Kinases (métabolisme), Glutarédoxines (MeSH), Glutathion (métabolisme), Glutathion (physiologie), Humains (MeSH), Lignée cellulaire (MeSH), Myocytes cardiaques (anatomopathologie), Myocytes cardiaques (métabolisme), Oxidoreductases (physiologie), Protéines G ras (génétique), Protéines G ras (métabolisme), Rats (MeSH), Spectrométrie de masse MALDI (méthodes), Système de signalisation des MAP kinases (MeSH), Transfection (MeSH).
- MESH :
- anatomopathologie : Myocytes cardiaques.
- biosynthèse : Extracellular Signal-Regulated MAP Kinases.
- composition chimique : Cystéine.
- génétique : Adenoviridae, Catalase, Protéines G ras.
- métabolisme : Cardiomyopathie hypertrophique, Extracellular Signal-Regulated MAP Kinases, Glutathion, Myocytes cardiaques, Protéines G ras.
- méthodes : Spectrométrie de masse MALDI.
- physiologie : Catalase, Glutathion, Oxidoreductases.
- étiologie : Cardiomyopathie hypertrophique.
- Animaux, Animaux nouveau-nés, Contrainte mécanique, Espèces réactives de l'oxygène, Glutarédoxines, Humains, Lignée cellulaire, Rats, Système de signalisation des MAP kinases, Transfection.
English descriptors
- KwdEn :
- Adenoviridae (genetics), Animals (MeSH), Animals, Newborn (MeSH), Cardiomyopathy, Hypertrophic (etiology), Cardiomyopathy, Hypertrophic (metabolism), Catalase (genetics), Catalase (physiology), Cell Line (MeSH), Cysteine (chemistry), Extracellular Signal-Regulated MAP Kinases (biosynthesis), Extracellular Signal-Regulated MAP Kinases (metabolism), Glutaredoxins (MeSH), Glutathione (metabolism), Glutathione (physiology), Humans (MeSH), MAP Kinase Signaling System (MeSH), Myocytes, Cardiac (metabolism), Myocytes, Cardiac (pathology), Oxidoreductases (physiology), Rats (MeSH), Reactive Oxygen Species (MeSH), Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization (methods), Stress, Mechanical (MeSH), Transfection (MeSH), ras Proteins (genetics), ras Proteins (metabolism).
- MESH :
- chemical , biosynthesis : Extracellular Signal-Regulated MAP Kinases.
- chemical , chemistry : Cysteine.
- chemical , genetics : Catalase, ras Proteins.
- etiology : Cardiomyopathy, Hypertrophic.
- genetics : Adenoviridae.
- metabolism : Cardiomyopathy, Hypertrophic, Extracellular Signal-Regulated MAP Kinases, Glutathione, Myocytes, Cardiac, ras Proteins.
- methods : Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization.
- pathology : Myocytes, Cardiac.
- chemical , physiology : Catalase, Glutathione, Oxidoreductases.
- Animals, Animals, Newborn, Cell Line, Glutaredoxins, Humans, MAP Kinase Signaling System, Rats, Reactive Oxygen Species, Stress, Mechanical, Transfection.
Abstract
Although reactive oxygen species (ROS) appear to play a central role in mediating myocardial hypertrophy in response to hemodynamic overload, little is known about the molecular targets by which ROS regulate growth signaling. In cardiac myocytes, we tested the hypothesis that mechanical strain causes cellular hypertrophy via ROS-dependent post-translational modification of Ras leading to activation of the Raf/Mek/Erk growth pathway. Cyclic mechanical strain increased Ras activity by 1.5 to 1.6-fold. Adenoviral overexpression of the N17 dominant negative mutant of Ras inhibited strain-stimulated Erk activation and protein synthesis. Strain-stimulated Ras activation was inhibited by overexpression of catalase, indicating that it is redox-dependent. Strain caused S-glutathiolation of Ras, which was inhibited by catalase overexpression and reversed by DTT. MALDI-TOF mass spectrometry demonstrated that in myocytes subjected to strain there was S-glutathiolation of Ras at Cys118. Adenoviral overexpression of a mutated Ras in which Cys118 was substituted with serine inhibited strain-stimulated S-glutathiolation of Ras, Erk activation and protein synthesis. Overexpression of glutaredoxin-1 likewise inhibited strain-stimulated Ras S-glutathiolation, Ras activation, Erk activation and protein synthesis. These findings indicate that mechanical strain causes ROS-dependent S-glutathiolation of Ras at Cys118, leading to myocyte hypertrophy via activation of the Raf/Mek/Erk pathway.
DOI: 10.1016/j.yjmcc.2006.05.009
PubMed: 16806262
Affiliations:
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Le document en format XML
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(metabolism)</term><term>Myocytes, Cardiac (pathology)</term><term>Oxidoreductases (physiology)</term><term>Rats (MeSH)</term><term>Reactive Oxygen Species (MeSH)</term><term>Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization (methods)</term><term>Stress, Mechanical (MeSH)</term><term>Transfection (MeSH)</term><term>ras Proteins (genetics)</term><term>ras Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adenoviridae (génétique)</term><term>Animaux (MeSH)</term><term>Animaux nouveau-nés (MeSH)</term><term>Cardiomyopathie hypertrophique (métabolisme)</term><term>Cardiomyopathie hypertrophique (étiologie)</term><term>Catalase (génétique)</term><term>Catalase (physiologie)</term><term>Contrainte mécanique (MeSH)</term><term>Cystéine (composition chimique)</term><term>Espèces réactives de l'oxygène (MeSH)</term><term>Extracellular Signal-Regulated MAP Kinases (biosynthèse)</term><term>Extracellular Signal-Regulated MAP Kinases (métabolisme)</term><term>Glutarédoxines (MeSH)</term><term>Glutathion (métabolisme)</term><term>Glutathion (physiologie)</term><term>Humains (MeSH)</term><term>Lignée cellulaire (MeSH)</term><term>Myocytes cardiaques (anatomopathologie)</term><term>Myocytes cardiaques (métabolisme)</term><term>Oxidoreductases (physiologie)</term><term>Protéines G ras (génétique)</term><term>Protéines G ras (métabolisme)</term><term>Rats (MeSH)</term><term>Spectrométrie de masse MALDI (méthodes)</term><term>Système de signalisation des MAP kinases (MeSH)</term><term>Transfection (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Extracellular Signal-Regulated MAP Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Cysteine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Catalase</term><term>ras Proteins</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Myocytes cardiaques</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Extracellular Signal-Regulated MAP Kinases</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Cystéine</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cardiomyopathy, Hypertrophic</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenoviridae</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Adenoviridae</term><term>Catalase</term><term>Protéines G ras</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cardiomyopathy, Hypertrophic</term><term>Extracellular Signal-Regulated MAP Kinases</term><term>Glutathione</term><term>Myocytes, Cardiac</term><term>ras Proteins</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cardiomyopathie hypertrophique</term><term>Extracellular Signal-Regulated MAP Kinases</term><term>Glutathion</term><term>Myocytes cardiaques</term><term>Protéines G ras</term></keywords><keywords scheme="MESH" qualifier="méthodes" xml:lang="fr"><term>Spectrométrie de masse MALDI</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Myocytes, Cardiac</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Catalase</term><term>Glutathion</term><term>Oxidoreductases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Catalase</term><term>Glutathione</term><term>Oxidoreductases</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Cardiomyopathie hypertrophique</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Animals, Newborn</term><term>Cell Line</term><term>Glutaredoxins</term><term>Humans</term><term>MAP Kinase Signaling System</term><term>Rats</term><term>Reactive Oxygen Species</term><term>Stress, Mechanical</term><term>Transfection</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Animaux nouveau-nés</term><term>Contrainte mécanique</term><term>Espèces réactives de l'oxygène</term><term>Glutarédoxines</term><term>Humains</term><term>Lignée cellulaire</term><term>Rats</term><term>Système de signalisation des MAP kinases</term><term>Transfection</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although reactive oxygen species (ROS) appear to play a central role in mediating myocardial hypertrophy in response to hemodynamic overload, little is known about the molecular targets by which ROS regulate growth signaling. In cardiac myocytes, we tested the hypothesis that mechanical strain causes cellular hypertrophy via ROS-dependent post-translational modification of Ras leading to activation of the Raf/Mek/Erk growth pathway. Cyclic mechanical strain increased Ras activity by 1.5 to 1.6-fold. Adenoviral overexpression of the N17 dominant negative mutant of Ras inhibited strain-stimulated Erk activation and protein synthesis. Strain-stimulated Ras activation was inhibited by overexpression of catalase, indicating that it is redox-dependent. Strain caused S-glutathiolation of Ras, which was inhibited by catalase overexpression and reversed by DTT. MALDI-TOF mass spectrometry demonstrated that in myocytes subjected to strain there was S-glutathiolation of Ras at Cys118. Adenoviral overexpression of a mutated Ras in which Cys118 was substituted with serine inhibited strain-stimulated S-glutathiolation of Ras, Erk activation and protein synthesis. Overexpression of glutaredoxin-1 likewise inhibited strain-stimulated Ras S-glutathiolation, Ras activation, Erk activation and protein synthesis. These findings indicate that mechanical strain causes ROS-dependent S-glutathiolation of Ras at Cys118, leading to myocyte hypertrophy via activation of the Raf/Mek/Erk pathway.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16806262</PMID><DateCompleted><Year>2007</Year><Month>01</Month><Day>12</Day></DateCompleted><DateRevised><Year>2020</Year><Month>02</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0022-2828</ISSN><JournalIssue CitedMedium="Print"><Volume>41</Volume><Issue>4</Issue><PubDate><Year>2006</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Journal of molecular and cellular cardiology</Title><ISOAbbreviation>J Mol Cell Cardiol</ISOAbbreviation></Journal><ArticleTitle>Strain-stimulated hypertrophy in cardiac myocytes is mediated by reactive oxygen species-dependent Ras S-glutathiolation.</ArticleTitle><Pagination><MedlinePgn>613-22</MedlinePgn></Pagination><Abstract><AbstractText>Although reactive oxygen species (ROS) appear to play a central role in mediating myocardial hypertrophy in response to hemodynamic overload, little is known about the molecular targets by which ROS regulate growth signaling. In cardiac myocytes, we tested the hypothesis that mechanical strain causes cellular hypertrophy via ROS-dependent post-translational modification of Ras leading to activation of the Raf/Mek/Erk growth pathway. Cyclic mechanical strain increased Ras activity by 1.5 to 1.6-fold. Adenoviral overexpression of the N17 dominant negative mutant of Ras inhibited strain-stimulated Erk activation and protein synthesis. Strain-stimulated Ras activation was inhibited by overexpression of catalase, indicating that it is redox-dependent. Strain caused S-glutathiolation of Ras, which was inhibited by catalase overexpression and reversed by DTT. MALDI-TOF mass spectrometry demonstrated that in myocytes subjected to strain there was S-glutathiolation of Ras at Cys118. Adenoviral overexpression of a mutated Ras in which Cys118 was substituted with serine inhibited strain-stimulated S-glutathiolation of Ras, Erk activation and protein synthesis. Overexpression of glutaredoxin-1 likewise inhibited strain-stimulated Ras S-glutathiolation, Ras activation, Erk activation and protein synthesis. These findings indicate that mechanical strain causes ROS-dependent S-glutathiolation of Ras at Cys118, leading to myocyte hypertrophy via activation of the Raf/Mek/Erk pathway.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pimentel</LastName><ForeName>David R</ForeName><Initials>DR</Initials><AffiliationInfo><Affiliation>Cardiovascular Medicine Section, Department of Medicine, Boston University Medical Center, Boston, MA 02118, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Adachi</LastName><ForeName>Takeshi</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Ido</LastName><ForeName>Yasuo</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Heibeck</LastName><ForeName>Tyler</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Bingbing</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Yong</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Melendez</LastName><ForeName>J Andres</ForeName><Initials>JA</Initials></Author><Author ValidYN="Y"><LastName>Cohen</LastName><ForeName>Richard A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Colucci</LastName><ForeName>Wilson S</ForeName><Initials>WS</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AG27080</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>CA95191</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>CA96989</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL007969</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL07224</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL20612</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL55620</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL61639</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01-HV-28178</GrantID><Acronym>HV</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2006</Year><Month>06</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Mol Cell Cardiol</MedlineTA><NlmUniqueID>0262322</NlmUniqueID><ISSNLinking>0022-2828</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C516007">Glrx protein, rat</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.-</RegistryNumber><NameOfSubstance UI="D010088">Oxidoreductases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.6</RegistryNumber><NameOfSubstance UI="D002374">Catalase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D048049">Extracellular Signal-Regulated MAP Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.5.2</RegistryNumber><NameOfSubstance UI="D018631">ras Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical><Chemical><RegistryNumber>K848JZ4886</RegistryNumber><NameOfSubstance UI="D003545">Cysteine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>J Mol Cell Cardiol. 2006 Oct;41(4):595-600</RefSource><PMID Version="1">16908028</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000256" MajorTopicYN="N">Adenoviridae</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" 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Signal-Regulated MAP Kinases</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020935" MajorTopicYN="Y">MAP Kinase Signaling System</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010088" MajorTopicYN="N">Oxidoreductases</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019032" MajorTopicYN="N">Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013314" MajorTopicYN="N">Stress, Mechanical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018631" MajorTopicYN="N">ras Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2005</Year><Month>09</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2006</Year><Month>05</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2006</Year><Month>05</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>6</Month><Day>30</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>1</Month><Day>16</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>6</Month><Day>30</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16806262</ArticleId><ArticleId IdType="pii">S0022-2828(06)00575-X</ArticleId><ArticleId IdType="doi">10.1016/j.yjmcc.2006.05.009</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region></list><tree><noCountry><name sortKey="Adachi, Takeshi" sort="Adachi, Takeshi" uniqKey="Adachi T" first="Takeshi" last="Adachi">Takeshi Adachi</name><name sortKey="Cohen, Richard A" sort="Cohen, Richard A" uniqKey="Cohen R" first="Richard A" last="Cohen">Richard A. Cohen</name><name sortKey="Colucci, Wilson S" sort="Colucci, Wilson S" uniqKey="Colucci W" first="Wilson S" last="Colucci">Wilson S. Colucci</name><name sortKey="Heibeck, Tyler" sort="Heibeck, Tyler" uniqKey="Heibeck T" first="Tyler" last="Heibeck">Tyler Heibeck</name><name sortKey="Ido, Yasuo" sort="Ido, Yasuo" uniqKey="Ido Y" first="Yasuo" last="Ido">Yasuo Ido</name><name sortKey="Jiang, Bingbing" sort="Jiang, Bingbing" uniqKey="Jiang B" first="Bingbing" last="Jiang">Bingbing Jiang</name><name sortKey="Lee, Yong" sort="Lee, Yong" uniqKey="Lee Y" first="Yong" last="Lee">Yong Lee</name><name sortKey="Melendez, J Andres" sort="Melendez, J Andres" uniqKey="Melendez J" first="J Andres" last="Melendez">J Andres Melendez</name></noCountry><country name="États-Unis"><region name="Massachusetts"><name sortKey="Pimentel, David R" sort="Pimentel, David R" uniqKey="Pimentel D" first="David R" last="Pimentel">David R. 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