Detection of the full-length transcript variant for neurokinin-1 receptor in human whole blood associated with enhanced reinforcement of clot by substance-P
Identifieur interne : 001166 ( Istex/Corpus ); précédent : 001165; suivant : 001167Detection of the full-length transcript variant for neurokinin-1 receptor in human whole blood associated with enhanced reinforcement of clot by substance-P
Auteurs : Toshiharu Azma ; Yuki Sugimoto ; Hiroyuki Kinoshita ; Taishin Ito ; Masanori Tsukamoto ; Hiroshi Hoshijima ; Masakazu Nakao ; Hirosato KikuchiSource :
- Journal of Thrombosis and Thrombolysis [ 0929-5305 ] ; 2012-05-01.
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- KwdEn :
Abstract
Abstract: We have recently reported that a neurotransmitter for pain, substance-P (SP), promotes platelet-dependent clot formation through neurokinin-1 receptors (NK1Rs), in which leukocytes appear to be involved (J Thromb Thrombolysis 2009;27:280–6). Two naturally occurring splice isoforms of NK1R with different signal transduction potency, namely the full-length and the truncated NK1Rs are identified. It is known that human leukocytes express truncated NK1Rs, while in vivo expression of the full-length NK1R has not yet been fully clarified. Modulatory effects of alternative splicing for NK1Rs on clot formation also remain to be evaluated. Expression of the transcript variant mRNA for NK1Rs in human whole blood (n = 20) was evaluated by real-time reverse transcription polymerase chain reaction (RT-PCR). A 15 min time series of the strength of clot, formed after reloading of calcium in citrated whole blood with or without SP (10 nM) and a NK1R antagonist Spantide (1 μM), was measured by using oscillating-probe viscoelastometry. The full-length transcript variant was detected in 5 samples among 20. SP significantly increased the clot strength while Spantide suppressed the SP-derived change. The extent of modulation by SP/NK1R pathway in a subgroup with expression of the full-length transcript variant was three times as potent as those in another subgroup without expression. We conclude that expression of the full-length transcript variant for NK1R can be detected in human whole blood and that such expression is associated with the enhanced reinforcement of clot by SP. Further study is required to nominate this mRNA as a biomarker for prothrombotic risks in painful conditions such as perioperative period.
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DOI: 10.1007/s11239-011-0650-1
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sort="Kinoshita, Hiroyuki" uniqKey="Kinoshita H" first="Hiroyuki" last="Kinoshita">Hiroyuki Kinoshita</name><affiliation><mods:affiliation>Department of Anesthesiology, Wakayama Medical University, Wakayama, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ito, Taishin" sort="Ito, Taishin" uniqKey="Ito T" first="Taishin" last="Ito">Taishin Ito</name><affiliation><mods:affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</mods:affiliation></affiliation></author><author><name sortKey="Tsukamoto, Masanori" sort="Tsukamoto, Masanori" uniqKey="Tsukamoto M" first="Masanori" last="Tsukamoto">Masanori Tsukamoto</name><affiliation><mods:affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hoshijima, Hiroshi" sort="Hoshijima, Hiroshi" uniqKey="Hoshijima H" 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azmacci@nifty.com</mods:affiliation></affiliation></author><author><name sortKey="Sugimoto, Yuki" sort="Sugimoto, Yuki" uniqKey="Sugimoto Y" first="Yuki" last="Sugimoto">Yuki Sugimoto</name><affiliation><mods:affiliation>Department of Anesthesiology, Hiroshima University Hospital, Hiroshima, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kinoshita, Hiroyuki" sort="Kinoshita, Hiroyuki" uniqKey="Kinoshita H" first="Hiroyuki" last="Kinoshita">Hiroyuki Kinoshita</name><affiliation><mods:affiliation>Department of Anesthesiology, Wakayama Medical University, Wakayama, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ito, Taishin" sort="Ito, Taishin" uniqKey="Ito T" first="Taishin" last="Ito">Taishin Ito</name><affiliation><mods:affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</mods:affiliation></affiliation></author><author><name sortKey="Tsukamoto, Masanori" sort="Tsukamoto, Masanori" uniqKey="Tsukamoto M" first="Masanori" last="Tsukamoto">Masanori Tsukamoto</name><affiliation><mods:affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hoshijima, Hiroshi" sort="Hoshijima, Hiroshi" uniqKey="Hoshijima H" first="Hiroshi" last="Hoshijima">Hiroshi Hoshijima</name><affiliation><mods:affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nakao, Masakazu" sort="Nakao, Masakazu" uniqKey="Nakao M" first="Masakazu" last="Nakao">Masakazu Nakao</name><affiliation><mods:affiliation>Department of Anesthesiology, Hiroshima General Hospital, Hatsukaichi, Hiroshima, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kikuchi, Hirosato" sort="Kikuchi, Hirosato" uniqKey="Kikuchi H" first="Hirosato" last="Kikuchi">Hirosato Kikuchi</name><affiliation><mods:affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Thrombosis and Thrombolysis</title><title level="j" type="sub">A Journal for Translation, Application and Therapeutics in Thrombosis and Vascular Science</title><title level="j" type="abbrev">J Thromb Thrombolysis</title><idno type="ISSN">0929-5305</idno><idno type="eISSN">1573-742X</idno><imprint><publisher>Springer US; http://www.springer-ny.com</publisher><pubPlace>Boston</pubPlace><date type="published" when="2012-05-01">2012-05-01</date><biblScope unit="volume">33</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="329">329</biblScope><biblScope unit="page" to="337">337</biblScope></imprint><idno 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Two naturally occurring splice isoforms of NK1R with different signal transduction potency, namely the full-length and the truncated NK1Rs are identified. It is known that human leukocytes express truncated NK1Rs, while in vivo expression of the full-length NK1R has not yet been fully clarified. Modulatory effects of alternative splicing for NK1Rs on clot formation also remain to be evaluated. Expression of the transcript variant mRNA for NK1Rs in human whole blood (n = 20) was evaluated by real-time reverse transcription polymerase chain reaction (RT-PCR). A 15 min time series of the strength of clot, formed after reloading of calcium in citrated whole blood with or without SP (10 nM) and a NK1R antagonist Spantide (1 μM), was measured by using oscillating-probe viscoelastometry. The full-length transcript variant was detected in 5 samples among 20. SP significantly increased the clot strength while Spantide suppressed the SP-derived change. The extent of modulation by SP/NK1R pathway in a subgroup with expression of the full-length transcript variant was three times as potent as those in another subgroup without expression. We conclude that expression of the full-length transcript variant for NK1R can be detected in human whole blood and that such expression is associated with the enhanced reinforcement of clot by SP. Further study is required to nominate this mRNA as a biomarker for prothrombotic risks in painful conditions such as perioperative period.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>Toshiharu Azma</name><affiliations><json:string>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</json:string><json:string>E-mail: azmacci@nifty.com</json:string></affiliations></json:item><json:item><name>Yuki Sugimoto</name><affiliations><json:string>Department of Anesthesiology, Hiroshima University Hospital, Hiroshima, Japan</json:string></affiliations></json:item><json:item><name>Hiroyuki Kinoshita</name><affiliations><json:string>Department of Anesthesiology, Wakayama Medical University, Wakayama, Japan</json:string></affiliations></json:item><json:item><name>Taishin Ito</name><affiliations><json:string>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</json:string></affiliations></json:item><json:item><name>Masanori Tsukamoto</name><affiliations><json:string>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</json:string></affiliations></json:item><json:item><name>Hiroshi Hoshijima</name><affiliations><json:string>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</json:string></affiliations></json:item><json:item><name>Masakazu Nakao</name><affiliations><json:string>Department of Anesthesiology, Hiroshima General Hospital, Hatsukaichi, Hiroshima, Japan</json:string></affiliations></json:item><json:item><name>Hirosato Kikuchi</name><affiliations><json:string>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Substance-P</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neurokinin-1 receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Transcript variant</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Splice isoform</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Clot formation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Leukocytes</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ANOVA : Analysis of variance</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CCL5 : Chemokine (C–C motif) ligand 5</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CD11b/CD18 (Mac-1) : Macrophage-1 antigen</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cDNA : Complementary deoxyribonucleic acid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Ct : Threshold cycle</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mRNA : Messenger ribonucleic acid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>NK1R : Neurokinin-1 receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PSGL1 : P-selectin glycoprotein ligand 1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>RT-PCR : Reverse transcription polymerase chain reaction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SP : Substance-P</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>t-PA : Tissue-plasminogen activator</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>VTE : Venous thromboembolism</value></json:item></subject><articleId><json:string>650</json:string><json:string>s11239-011-0650-1</json:string></articleId><arkIstex>ark:/67375/VQC-XM2CJ1CT-3</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>OriginalPaper</json:string></originalGenre><abstract>Abstract: We have recently reported that a neurotransmitter for pain, substance-P (SP), promotes platelet-dependent clot formation through neurokinin-1 receptors (NK1Rs), in which leukocytes appear to be involved (J Thromb Thrombolysis 2009;27:280–6). Two naturally occurring splice isoforms of NK1R with different signal transduction potency, namely the full-length and the truncated NK1Rs are identified. It is known that human leukocytes express truncated NK1Rs, while in vivo expression of the full-length NK1R has not yet been fully clarified. Modulatory effects of alternative splicing for NK1Rs on clot formation also remain to be evaluated. Expression of the transcript variant mRNA for NK1Rs in human whole blood (n = 20) was evaluated by real-time reverse transcription polymerase chain reaction (RT-PCR). A 15 min time series of the strength of clot, formed after reloading of calcium in citrated whole blood with or without SP (10 nM) and a NK1R antagonist Spantide (1 μM), was measured by using oscillating-probe viscoelastometry. The full-length transcript variant was detected in 5 samples among 20. SP significantly increased the clot strength while Spantide suppressed the SP-derived change. The extent of modulation by SP/NK1R pathway in a subgroup with expression of the full-length transcript variant was three times as potent as those in another subgroup without expression. We conclude that expression of the full-length transcript variant for NK1R can be detected in human whole blood and that such expression is associated with the enhanced reinforcement of clot by SP. Further study is required to nominate this mRNA as a biomarker for prothrombotic risks in painful conditions such as perioperative period.</abstract><qualityIndicators><refBibsNative>false</refBibsNative><abstractWordCount>253</abstractWordCount><abstractCharCount>1732</abstractCharCount><keywordCount>18</keywordCount><score>10</score><pdfWordCount>5475</pdfWordCount><pdfCharCount>34576</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>595.276 x 790.866 pts</pdfPageSize></qualityIndicators><title>Detection of the full-length transcript variant for neurokinin-1 receptor in human whole blood associated with enhanced reinforcement of clot by substance-P</title><genre><json:string>research-article</json:string></genre><host><title>Journal of Thrombosis and Thrombolysis</title><language><json:string>unknown</json:string></language><publicationDate>2012</publicationDate><copyrightDate>2012</copyrightDate><issn><json:string>0929-5305</json:string></issn><eissn><json:string>1573-742X</json:string></eissn><journalId><json:string>11239</json:string></journalId><volume>33</volume><issue>4</issue><pages><first>329</first><last>337</last></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Cardiology</value></json:item><json:item><value>Hematology</value></json:item></subject></host><ark><json:string>ark:/67375/VQC-XM2CJ1CT-3</json:string></ark><publicationDate>2012</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1007/s11239-011-0650-1</json:string></doi><id>553766C59B379F19FD329028DDE09EA12D4AA4AC</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-XM2CJ1CT-3/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-XM2CJ1CT-3/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/VQC-XM2CJ1CT-3/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Detection of the full-length transcript variant for neurokinin-1 receptor in human whole blood associated with enhanced reinforcement of clot by substance-P</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">Springer US; 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http://www.springer-ny.com</publisher><pubPlace>Boston</pubPlace><date type="published" when="2012-05-01"></date><biblScope unit="volume">33</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="329">329</biblScope><biblScope unit="page" to="337">337</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: We have recently reported that a neurotransmitter for pain, substance-P (SP), promotes platelet-dependent clot formation through neurokinin-1 receptors (NK1Rs), in which leukocytes appear to be involved (J Thromb Thrombolysis 2009;27:280–6). Two naturally occurring splice isoforms of NK1R with different signal transduction potency, namely the full-length and the truncated NK1Rs are identified. It is known that human leukocytes express truncated NK1Rs, while in vivo expression of the full-length NK1R has not yet been fully clarified. Modulatory effects of alternative splicing for NK1Rs on clot formation also remain to be evaluated. Expression of the transcript variant mRNA for NK1Rs in human whole blood (n = 20) was evaluated by real-time reverse transcription polymerase chain reaction (RT-PCR). A 15 min time series of the strength of clot, formed after reloading of calcium in citrated whole blood with or without SP (10 nM) and a NK1R antagonist Spantide (1 μM), was measured by using oscillating-probe viscoelastometry. The full-length transcript variant was detected in 5 samples among 20. SP significantly increased the clot strength while Spantide suppressed the SP-derived change. The extent of modulation by SP/NK1R pathway in a subgroup with expression of the full-length transcript variant was three times as potent as those in another subgroup without expression. We conclude that expression of the full-length transcript variant for NK1R can be detected in human whole blood and that such expression is associated with the enhanced reinforcement of clot by SP. Further study is required to nominate this mRNA as a biomarker for prothrombotic risks in painful conditions such as perioperative period.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Substance-P</term></item><item><term>Neurokinin-1 receptor</term></item><item><term>Transcript variant</term></item><item><term>Splice isoform</term></item><item><term>Clot formation</term></item><item><term>Leukocytes</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>Abbreviations</head><item><term>ANOVA</term><term>Analysis of variance</term></item><item><term>CCL5</term><term>Chemokine (C–C motif) ligand 5</term></item><item><term>CD11b/CD18 (Mac-1)</term><term>Macrophage-1 antigen</term></item><item><term>cDNA</term><term>Complementary deoxyribonucleic acid</term></item><item><term>Ct</term><term>Threshold cycle</term></item><item><term>mRNA</term><term>Messenger ribonucleic acid</term></item><item><term>NK1R</term><term>Neurokinin-1 receptor</term></item><item><term>PSGL1</term><term>P-selectin glycoprotein ligand 1</term></item><item><term>RT-PCR</term><term>Reverse transcription polymerase chain reaction</term></item><item><term>SP</term><term>Substance-P</term></item><item><term>t-PA</term><term>Tissue-plasminogen activator</term></item><item><term>VTE</term><term>Venous thromboembolism</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Cardiology</term></item><item><term>Hematology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2012-05-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-XM2CJ1CT-3/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus springer-journals not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer US</PublisherName><PublisherLocation>Boston</PublisherLocation><PublisherURL>http://www.springer-ny.com</PublisherURL></PublisherInfo><Journal OutputMedium="All"><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>11239</JournalID><JournalPrintISSN>0929-5305</JournalPrintISSN><JournalElectronicISSN>1573-742X</JournalElectronicISSN><JournalTitle>Journal of Thrombosis and Thrombolysis</JournalTitle><JournalSubTitle>A Journal for Translation, Application and Therapeutics in Thrombosis and Vascular Science</JournalSubTitle><JournalAbbreviatedTitle>J Thromb Thrombolysis</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Medicine & Public Health</JournalSubject><JournalSubject Type="Secondary">Cardiology</JournalSubject><JournalSubject Type="Secondary">Hematology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume OutputMedium="All"><VolumeInfo TocLevels="0" VolumeType="Regular"><VolumeIDStart>33</VolumeIDStart><VolumeIDEnd>33</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular" OutputMedium="All"><IssueInfo IssueType="Regular" TocLevels="0"><IssueIDStart>4</IssueIDStart><IssueIDEnd>4</IssueIDEnd><IssueTitle Language="En">Special Issue on Biomarker Science: At the Interface of Systems-Based Biology, Pharmacology and Phenomics</IssueTitle><IssueArticleCount>16</IssueArticleCount><IssueHistory><OnlineDate><Year>2012</Year><Month>4</Month><Day>27</Day></OnlineDate><PrintDate><Year>2012</Year><Month>4</Month><Day>26</Day></PrintDate><CoverDate><Year>2012</Year><Month>5</Month></CoverDate><PricelistYear>2012</PricelistYear></IssueHistory><IssueCopyright><CopyrightHolderName>Springer Science+Business Media, LLC</CopyrightHolderName><CopyrightYear>2012</CopyrightYear></IssueCopyright></IssueInfo><Article ID="s11239-011-0650-1" OutputMedium="All"><ArticleInfo ArticleType="OriginalPaper" ContainsESM="No" Language="En" NumberingStyle="Unnumbered" TocLevels="0"><ArticleID>650</ArticleID><ArticleDOI>10.1007/s11239-011-0650-1</ArticleDOI><ArticleSequenceNumber>5</ArticleSequenceNumber><ArticleTitle Language="En" OutputMedium="All">Detection of the full-length transcript variant for neurokinin-1 receptor in human whole blood associated with enhanced reinforcement of clot by substance-P</ArticleTitle><ArticleFirstPage>329</ArticleFirstPage><ArticleLastPage>337</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2011</Year><Month>10</Month><Day>25</Day></RegistrationDate><OnlineDate><Year>2011</Year><Month>11</Month><Day>5</Day></OnlineDate></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer Science+Business Media, LLC</CopyrightHolderName><CopyrightYear>2011</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Toshiharu</GivenName><FamilyName>Azma</FamilyName></AuthorName><Contact><Phone>+81-49-276-1271</Phone><Fax>+81-49-276-1271</Fax><Email>azmacci@nifty.com</Email></Contact></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Yuki</GivenName><FamilyName>Sugimoto</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>Hiroyuki</GivenName><FamilyName>Kinoshita</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Taishin</GivenName><FamilyName>Ito</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Masanori</GivenName><FamilyName>Tsukamoto</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Hiroshi</GivenName><FamilyName>Hoshijima</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4"><AuthorName DisplayOrder="Western"><GivenName>Masakazu</GivenName><FamilyName>Nakao</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Hirosato</GivenName><FamilyName>Kikuchi</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Department of Anesthesiology, Faculty of Medicine</OrgDivision><OrgName>Saitama Medical University</OrgName><OrgAddress><Street>Iruma-gun</Street><City>Saitama</City><Postcode>350-0495</Postcode><Country Code="JP">Japan</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Department of Anesthesiology</OrgDivision><OrgName>Hiroshima University Hospital</OrgName><OrgAddress><City>Hiroshima</City><Country Code="JP">Japan</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Department of Anesthesiology</OrgDivision><OrgName>Wakayama Medical University</OrgName><OrgAddress><City>Wakayama</City><Country Code="JP">Japan</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Department of Anesthesiology</OrgDivision><OrgName>Hiroshima General Hospital</OrgName><OrgAddress><Street>Hatsukaichi</Street><City>Hiroshima</City><Country Code="JP">Japan</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En" OutputMedium="All"><Heading>Abstract</Heading><Para>We have recently reported that a neurotransmitter for pain, substance-P (SP), promotes platelet-dependent clot formation through neurokinin-1 receptors (NK1Rs), in which leukocytes appear to be involved (J Thromb Thrombolysis 2009;27:280–6). Two naturally occurring splice isoforms of NK1R with different signal transduction potency, namely the full-length and the truncated NK1Rs are identified. It is known that human leukocytes express truncated NK1Rs, while in vivo expression of the full-length NK1R has not yet been fully clarified. Modulatory effects of alternative splicing for NK1Rs on clot formation also remain to be evaluated. Expression of the transcript variant mRNA for NK1Rs in human whole blood (<Emphasis Type="Italic">n</Emphasis> = 20) was evaluated by real-time reverse transcription polymerase chain reaction (RT-PCR). A 15 min time series of the strength of clot, formed after reloading of calcium in citrated whole blood with or without SP (10 nM) and a NK1R antagonist Spantide (1 μM), was measured by using oscillating-probe viscoelastometry. The full-length transcript variant was detected in 5 samples among 20. SP significantly increased the clot strength while Spantide suppressed the SP-derived change. The extent of modulation by SP/NK1R pathway in a subgroup with expression of the full-length transcript variant was three times as potent as those in another subgroup without expression. We conclude that expression of the full-length transcript variant for NK1R can be detected in human whole blood and that such expression is associated with the enhanced reinforcement of clot by SP. Further study is required to nominate this mRNA as a biomarker for prothrombotic risks in painful conditions such as perioperative period.</Para></Abstract><KeywordGroup Language="En" OutputMedium="All"><Heading>Keywords</Heading><Keyword>Substance-P</Keyword><Keyword>Neurokinin-1 receptor</Keyword><Keyword>Transcript variant</Keyword><Keyword>Splice isoform</Keyword><Keyword>Clot formation</Keyword><Keyword>Leukocytes</Keyword></KeywordGroup><AbbreviationGroup><Heading>Abbreviations</Heading><DefinitionList><DefinitionListEntry><Term>ANOVA</Term><Description><Para>Analysis of variance</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>CCL5</Term><Description><Para>Chemokine (C–C motif) ligand 5</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>CD11b/CD18 (Mac-1)</Term><Description><Para>Macrophage-1 antigen</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>cDNA</Term><Description><Para>Complementary deoxyribonucleic acid</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>Ct</Term><Description><Para>Threshold cycle</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>mRNA</Term><Description><Para>Messenger ribonucleic acid</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>NK1R</Term><Description><Para>Neurokinin-1 receptor</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>PSGL1</Term><Description><Para>P-selectin glycoprotein ligand 1</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>RT-PCR</Term><Description><Para>Reverse transcription polymerase chain reaction</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>SP</Term><Description><Para>Substance-P</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>t-PA</Term><Description><Para>Tissue-plasminogen activator</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>VTE</Term><Description><Para>Venous thromboembolism</Para></Description></DefinitionListEntry></DefinitionList></AbbreviationGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Detection of the full-length transcript variant for neurokinin-1 receptor in human whole blood associated with enhanced reinforcement of clot by substance-P</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Detection of the full-length transcript variant for neurokinin-1 receptor in human whole blood associated with enhanced reinforcement of clot by substance-P</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Toshiharu</namePart><namePart type="family">Azma</namePart><affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</affiliation><affiliation>E-mail: azmacci@nifty.com</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yuki</namePart><namePart type="family">Sugimoto</namePart><affiliation>Department of Anesthesiology, Hiroshima University Hospital, Hiroshima, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroyuki</namePart><namePart type="family">Kinoshita</namePart><affiliation>Department of Anesthesiology, Wakayama Medical University, Wakayama, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Taishin</namePart><namePart type="family">Ito</namePart><affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Masanori</namePart><namePart type="family">Tsukamoto</namePart><affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroshi</namePart><namePart type="family">Hoshijima</namePart><affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Masakazu</namePart><namePart type="family">Nakao</namePart><affiliation>Department of Anesthesiology, Hiroshima General Hospital, Hatsukaichi, Hiroshima, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hirosato</namePart><namePart type="family">Kikuchi</namePart><affiliation>Department of Anesthesiology, Faculty of Medicine, Saitama Medical University, Iruma-gun, 350-0495, Saitama, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>Springer US; http://www.springer-ny.com</publisher><place><placeTerm type="text">Boston</placeTerm></place><dateIssued encoding="w3cdtf">2012-05-01</dateIssued><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: We have recently reported that a neurotransmitter for pain, substance-P (SP), promotes platelet-dependent clot formation through neurokinin-1 receptors (NK1Rs), in which leukocytes appear to be involved (J Thromb Thrombolysis 2009;27:280–6). Two naturally occurring splice isoforms of NK1R with different signal transduction potency, namely the full-length and the truncated NK1Rs are identified. It is known that human leukocytes express truncated NK1Rs, while in vivo expression of the full-length NK1R has not yet been fully clarified. Modulatory effects of alternative splicing for NK1Rs on clot formation also remain to be evaluated. Expression of the transcript variant mRNA for NK1Rs in human whole blood (n = 20) was evaluated by real-time reverse transcription polymerase chain reaction (RT-PCR). A 15 min time series of the strength of clot, formed after reloading of calcium in citrated whole blood with or without SP (10 nM) and a NK1R antagonist Spantide (1 μM), was measured by using oscillating-probe viscoelastometry. The full-length transcript variant was detected in 5 samples among 20. SP significantly increased the clot strength while Spantide suppressed the SP-derived change. The extent of modulation by SP/NK1R pathway in a subgroup with expression of the full-length transcript variant was three times as potent as those in another subgroup without expression. We conclude that expression of the full-length transcript variant for NK1R can be detected in human whole blood and that such expression is associated with the enhanced reinforcement of clot by SP. Further study is required to nominate this mRNA as a biomarker for prothrombotic risks in painful conditions such as perioperative period.</abstract><subject lang="en"><genre>Keywords</genre><topic>Substance-P</topic><topic>Neurokinin-1 receptor</topic><topic>Transcript variant</topic><topic>Splice isoform</topic><topic>Clot formation</topic><topic>Leukocytes</topic></subject><subject><genre>Abbreviations</genre><topic>ANOVA : Analysis of variance</topic><topic>CCL5 : Chemokine (C–C motif) ligand 5</topic><topic>CD11b/CD18 (Mac-1) : Macrophage-1 antigen</topic><topic>cDNA : Complementary deoxyribonucleic acid</topic><topic>Ct : Threshold cycle</topic><topic>mRNA : Messenger ribonucleic acid</topic><topic>NK1R : Neurokinin-1 receptor</topic><topic>PSGL1 : P-selectin glycoprotein ligand 1</topic><topic>RT-PCR : Reverse transcription polymerase chain reaction</topic><topic>SP : Substance-P</topic><topic>t-PA : Tissue-plasminogen activator</topic><topic>VTE : Venous thromboembolism</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Thrombosis and Thrombolysis</title><subTitle>A Journal for Translation, Application and Therapeutics in Thrombosis and Vascular Science</subTitle></titleInfo><titleInfo type="abbreviated"><title>J Thromb Thrombolysis</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">2012-04-27</dateIssued><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Cardiology</topic><topic>Hematology</topic></subject><identifier type="ISSN">0929-5305</identifier><identifier type="eISSN">1573-742X</identifier><identifier type="JournalID">11239</identifier><identifier type="IssueArticleCount">16</identifier><identifier type="VolumeIssueCount">4</identifier><part><date>2012</date><detail type="issue"><title>Special Issue on Biomarker Science: At the Interface of Systems-Based Biology, Pharmacology and Phenomics</title></detail><detail type="volume"><number>33</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="pages"><start>329</start><end>337</end></extent></part><recordInfo><recordOrigin>Springer Science+Business Media, LLC, 2012</recordOrigin></recordInfo></relatedItem><identifier type="istex">553766C59B379F19FD329028DDE09EA12D4AA4AC</identifier><identifier type="ark">ark:/67375/VQC-XM2CJ1CT-3</identifier><identifier type="DOI">10.1007/s11239-011-0650-1</identifier><identifier type="ArticleID">650</identifier><identifier type="ArticleID">s11239-011-0650-1</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer Science+Business Media, LLC, 2011</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Springer Science+Business Media, LLC, 2011</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-XM2CJ1CT-3/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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