Hemostatic disorders in a JAK2V617F-driven mouse model of myeloproliferative neoplasm.
Identifieur interne : 003508 ( PubMed/Checkpoint ); précédent : 003507; suivant : 003509Hemostatic disorders in a JAK2V617F-driven mouse model of myeloproliferative neoplasm.
Auteurs : Lamia Lamrani [France] ; Catherine Lacout [France] ; Véronique Ollivier [France] ; Cécile V. Denis ; Elizabeth Gardiner [Australie] ; Benoit Ho Tin Noe [France] ; William Vainchenker [France] ; Jean-Luc Villeval [France] ; Martine Jandrot-Perrus [France]Source :
- Blood [ 1528-0020 ] ; 2014.
Descripteurs français
- KwdFr :
- Activation plaquettaire (génétique), Animaux, Aorte (anatomopathologie), Aorte (métabolisme), Aorte (physiopathologie), Cytométrie en flux, Facteur de von Willebrand (métabolisme), Glycoprotéines de membrane plaquettaire (génétique), Glycoprotéines de membrane plaquettaire (métabolisme), Humains, Immunotransfert, Kinase Janus-2 (génétique), Modèles animaux de maladie humaine, Mutation faux-sens, Myélofibrose primitive (génétique), Myélofibrose primitive (sang), Plaquettes (métabolisme), Polyglobulie primitive essentielle (génétique), Polyglobulie primitive essentielle (sang), Souris transgéniques, Syndromes myéloprolifératifs (génétique), Syndromes myéloprolifératifs (sang), Techniques de knock-in de gènes, Temps de saignement, Thrombose (génétique), Thrombose (sang), Troubles de l'hémostase (génétique), Vasodilatation (génétique).
- MESH :
- anatomopathologie : Aorte.
- génétique : Activation plaquettaire, Glycoprotéines de membrane plaquettaire, Kinase Janus-2, Myélofibrose primitive, Polyglobulie primitive essentielle, Syndromes myéloprolifératifs, Thrombose, Troubles de l'hémostase, Vasodilatation.
- métabolisme : Aorte, Facteur de von Willebrand, Glycoprotéines de membrane plaquettaire, Plaquettes.
- physiopathologie : Aorte.
- sang : Myélofibrose primitive, Polyglobulie primitive essentielle, Syndromes myéloprolifératifs, Thrombose.
- Animaux, Cytométrie en flux, Humains, Immunotransfert, Modèles animaux de maladie humaine, Mutation faux-sens, Souris transgéniques, Techniques de knock-in de gènes, Temps de saignement.
English descriptors
- KwdEn :
- Animals, Aorta (metabolism), Aorta (pathology), Aorta (physiopathology), Bleeding Time, Blood Platelets (metabolism), Disease Models, Animal, Flow Cytometry, Gene Knock-In Techniques, Hemostatic Disorders (genetics), Humans, Immunoblotting, Janus Kinase 2 (genetics), Mice, Transgenic, Mutation, Missense, Myeloproliferative Disorders (blood), Myeloproliferative Disorders (genetics), Platelet Activation (genetics), Platelet Membrane Glycoproteins (genetics), Platelet Membrane Glycoproteins (metabolism), Polycythemia Vera (blood), Polycythemia Vera (genetics), Primary Myelofibrosis (blood), Primary Myelofibrosis (genetics), Thrombosis (blood), Thrombosis (genetics), Vasodilation (genetics), von Willebrand Factor (metabolism).
- MESH :
- chemical , genetics : Janus Kinase 2, Platelet Membrane Glycoproteins.
- blood : Myeloproliferative Disorders, Polycythemia Vera, Primary Myelofibrosis, Thrombosis.
- genetics : Hemostatic Disorders, Myeloproliferative Disorders, Platelet Activation, Polycythemia Vera, Primary Myelofibrosis, Thrombosis, Vasodilation.
- metabolism : Aorta, Blood Platelets, Platelet Membrane Glycoproteins, von Willebrand Factor.
- pathology : Aorta.
- physiopathology : Aorta.
- Animals, Bleeding Time, Disease Models, Animal, Flow Cytometry, Gene Knock-In Techniques, Humans, Immunoblotting, Mice, Transgenic, Mutation, Missense.
Abstract
Thrombosis is common in patients suffering from myeloproliferative neoplasm (MPN), whereas bleeding is less frequent. JAK2(V617F), the main mutation involved in MPN, is considered as a risk factor for thrombosis, although the direct link between the mutation and hemostatic disorders is not strictly established. We investigated this question using conditional JAK2(V617F) knock-in mice with constitutive and inducible expression of JAK2(V617F) in hematopoietic cells, which develop a polycythemia vera (PV)-like disorder evolving into myelofibrosis. In vitro, thrombosis was markedly impaired with an 80% decrease in platelet-covered surface, when JAK2(V617F) blood was perfused at arterial shear over collagen. JAK2(V617F) platelets presented only a moderate glycoprotein (GP) VI deficiency not responsible for the defective platelet accumulation. In contrast, a decreased proportion of high-molecular-weight von Willebrand factor multimers could reduce platelet adhesion. Accordingly, the tail bleeding time was prolonged. In the FeCl3-induced thrombosis model, platelet aggregates formed rapidly but were highly unstable. Interestingly, vessels were considerably dilated. Thus, mice developing PV secondary to constitutive JAK2(V617F) expression exhibit a bleeding tendency combined with the accelerated formation of unstable clots, reminiscent of observations made in patients. Hemostatic defects were not concomitant with the induction of JAK2(V617F) expression, suggesting they were not directly caused by the mutation but were rather the consequence of perturbations in blood and vessel homeostasis.
DOI: 10.1182/blood-2013-10-530832
PubMed: 24951423
Affiliations:
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pubmed:24951423Le document en format XML
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<term>Aorta (metabolism)</term>
<term>Aorta (pathology)</term>
<term>Aorta (physiopathology)</term>
<term>Bleeding Time</term>
<term>Blood Platelets (metabolism)</term>
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<term>Facteur de von Willebrand (métabolisme)</term>
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<term>Glycoprotéines de membrane plaquettaire (métabolisme)</term>
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<term>Myeloproliferative Disorders</term>
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<term>Thrombosis</term>
<term>Vasodilation</term>
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<term>Syndromes myéloprolifératifs</term>
<term>Thrombose</term>
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<term>Bleeding Time</term>
<term>Disease Models, Animal</term>
<term>Flow Cytometry</term>
<term>Gene Knock-In Techniques</term>
<term>Humans</term>
<term>Immunoblotting</term>
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<term>Mutation, Missense</term>
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<term>Mutation faux-sens</term>
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<front><div type="abstract" xml:lang="en">Thrombosis is common in patients suffering from myeloproliferative neoplasm (MPN), whereas bleeding is less frequent. JAK2(V617F), the main mutation involved in MPN, is considered as a risk factor for thrombosis, although the direct link between the mutation and hemostatic disorders is not strictly established. We investigated this question using conditional JAK2(V617F) knock-in mice with constitutive and inducible expression of JAK2(V617F) in hematopoietic cells, which develop a polycythemia vera (PV)-like disorder evolving into myelofibrosis. In vitro, thrombosis was markedly impaired with an 80% decrease in platelet-covered surface, when JAK2(V617F) blood was perfused at arterial shear over collagen. JAK2(V617F) platelets presented only a moderate glycoprotein (GP) VI deficiency not responsible for the defective platelet accumulation. In contrast, a decreased proportion of high-molecular-weight von Willebrand factor multimers could reduce platelet adhesion. Accordingly, the tail bleeding time was prolonged. In the FeCl3-induced thrombosis model, platelet aggregates formed rapidly but were highly unstable. Interestingly, vessels were considerably dilated. Thus, mice developing PV secondary to constitutive JAK2(V617F) expression exhibit a bleeding tendency combined with the accelerated formation of unstable clots, reminiscent of observations made in patients. Hemostatic defects were not concomitant with the induction of JAK2(V617F) expression, suggesting they were not directly caused by the mutation but were rather the consequence of perturbations in blood and vessel homeostasis.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24951423</PMID>
<DateCreated><Year>2014</Year>
<Month>08</Month>
<Day>15</Day>
</DateCreated>
<DateCompleted><Year>2015</Year>
<Month>04</Month>
<Day>27</Day>
</DateCompleted>
<DateRevised><Year>2015</Year>
<Month>08</Month>
<Day>05</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1528-0020</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>124</Volume>
<Issue>7</Issue>
<PubDate><Year>2014</Year>
<Month>Aug</Month>
<Day>14</Day>
</PubDate>
</JournalIssue>
<Title>Blood</Title>
<ISOAbbreviation>Blood</ISOAbbreviation>
</Journal>
<ArticleTitle>Hemostatic disorders in a JAK2V617F-driven mouse model of myeloproliferative neoplasm.</ArticleTitle>
<Pagination><MedlinePgn>1136-45</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1182/blood-2013-10-530832</ELocationID>
<Abstract><AbstractText>Thrombosis is common in patients suffering from myeloproliferative neoplasm (MPN), whereas bleeding is less frequent. JAK2(V617F), the main mutation involved in MPN, is considered as a risk factor for thrombosis, although the direct link between the mutation and hemostatic disorders is not strictly established. We investigated this question using conditional JAK2(V617F) knock-in mice with constitutive and inducible expression of JAK2(V617F) in hematopoietic cells, which develop a polycythemia vera (PV)-like disorder evolving into myelofibrosis. In vitro, thrombosis was markedly impaired with an 80% decrease in platelet-covered surface, when JAK2(V617F) blood was perfused at arterial shear over collagen. JAK2(V617F) platelets presented only a moderate glycoprotein (GP) VI deficiency not responsible for the defective platelet accumulation. In contrast, a decreased proportion of high-molecular-weight von Willebrand factor multimers could reduce platelet adhesion. Accordingly, the tail bleeding time was prolonged. In the FeCl3-induced thrombosis model, platelet aggregates formed rapidly but were highly unstable. Interestingly, vessels were considerably dilated. Thus, mice developing PV secondary to constitutive JAK2(V617F) expression exhibit a bleeding tendency combined with the accelerated formation of unstable clots, reminiscent of observations made in patients. Hemostatic defects were not concomitant with the induction of JAK2(V617F) expression, suggesting they were not directly caused by the mutation but were rather the consequence of perturbations in blood and vessel homeostasis.</AbstractText>
<CopyrightInformation>© 2014 by The American Society of Hematology.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lamrani</LastName>
<ForeName>Lamia</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>INSERM, U1148, Paris, France; Université Paris Denis Diderot 7, Paris, France;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lacout</LastName>
<ForeName>Catherine</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>INSERM, U1009, Villejuif, France; Université Paris-Sud 11, Villejuif, France; Institut Gustave Roussy, Villejuif, France;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ollivier</LastName>
<ForeName>Véronique</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>INSERM, U1148, Paris, France; Université Paris Denis Diderot 7, Paris, France;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Denis</LastName>
<ForeName>Cécile V</ForeName>
<Initials>CV</Initials>
<AffiliationInfo><Affiliation>Université Paris-Sud 11, Villejuif, France; INSERM, U770, Le Kremlin-Bicêtre, France; and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gardiner</LastName>
<ForeName>Elizabeth</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Monash University, Clayton, VIC, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ho Tin Noe</LastName>
<ForeName>Benoit</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>INSERM, U1148, Paris, France; Université Paris Denis Diderot 7, Paris, France;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Vainchenker</LastName>
<ForeName>William</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>INSERM, U1009, Villejuif, France; Université Paris-Sud 11, Villejuif, France; Institut Gustave Roussy, Villejuif, France;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Villeval</LastName>
<ForeName>Jean-Luc</ForeName>
<Initials>JL</Initials>
<AffiliationInfo><Affiliation>INSERM, U1009, Villejuif, France; Université Paris-Sud 11, Villejuif, France; Institut Gustave Roussy, Villejuif, France;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jandrot-Perrus</LastName>
<ForeName>Martine</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>INSERM, U1148, Paris, France; Université Paris Denis Diderot 7, Paris, France;</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>2014</Year>
<Month>06</Month>
<Day>20</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Blood</MedlineTA>
<NlmUniqueID>7603509</NlmUniqueID>
<ISSNLinking>0006-4971</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D010980">Platelet Membrane Glycoproteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C098341">platelet membrane glycoprotein VI</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014841">von Willebrand Factor</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.2</RegistryNumber>
<NameOfSubstance UI="D053614">Janus Kinase 2</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>AIM</CitationSubset>
<CitationSubset>IM</CitationSubset>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001011" MajorTopicYN="N">Aorta</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001760" MajorTopicYN="N">Bleeding Time</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001792" MajorTopicYN="N">Blood Platelets</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="Y">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D055879" MajorTopicYN="N">Gene Knock-In Techniques</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020141" MajorTopicYN="N">Hemostatic Disorders</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015151" MajorTopicYN="N">Immunoblotting</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053614" MajorTopicYN="N">Janus Kinase 2</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D020125" MajorTopicYN="Y">Mutation, Missense</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009196" MajorTopicYN="N">Myeloproliferative Disorders</DescriptorName>
<QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015539" MajorTopicYN="N">Platelet Activation</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D010980" MajorTopicYN="N">Platelet Membrane Glycoproteins</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011087" MajorTopicYN="N">Polycythemia Vera</DescriptorName>
<QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D055728" MajorTopicYN="N">Primary Myelofibrosis</DescriptorName>
<QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013927" MajorTopicYN="N">Thrombosis</DescriptorName>
<QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014664" MajorTopicYN="N">Vasodilation</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D014841" MajorTopicYN="N">von Willebrand Factor</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<OtherID Source="NLM">PMC4133486</OtherID>
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<ArticleIdList><ArticleId IdType="pubmed">24951423</ArticleId>
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<affiliations><list><country><li>Australie</li>
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<settlement><li>Paris</li>
</settlement>
</list>
<tree><noCountry><name sortKey="Denis, Cecile V" sort="Denis, Cecile V" uniqKey="Denis C" first="Cécile V" last="Denis">Cécile V. Denis</name>
</noCountry>
<country name="France"><region name="Île-de-France"><name sortKey="Lamrani, Lamia" sort="Lamrani, Lamia" uniqKey="Lamrani L" first="Lamia" last="Lamrani">Lamia Lamrani</name>
</region>
<name sortKey="Ho Tin Noe, Benoit" sort="Ho Tin Noe, Benoit" uniqKey="Ho Tin Noe B" first="Benoit" last="Ho Tin Noe">Benoit Ho Tin Noe</name>
<name sortKey="Jandrot Perrus, Martine" sort="Jandrot Perrus, Martine" uniqKey="Jandrot Perrus M" first="Martine" last="Jandrot-Perrus">Martine Jandrot-Perrus</name>
<name sortKey="Lacout, Catherine" sort="Lacout, Catherine" uniqKey="Lacout C" first="Catherine" last="Lacout">Catherine Lacout</name>
<name sortKey="Ollivier, Veronique" sort="Ollivier, Veronique" uniqKey="Ollivier V" first="Véronique" last="Ollivier">Véronique Ollivier</name>
<name sortKey="Vainchenker, William" sort="Vainchenker, William" uniqKey="Vainchenker W" first="William" last="Vainchenker">William Vainchenker</name>
<name sortKey="Villeval, Jean Luc" sort="Villeval, Jean Luc" uniqKey="Villeval J" first="Jean-Luc" last="Villeval">Jean-Luc Villeval</name>
</country>
<country name="Australie"><noRegion><name sortKey="Gardiner, Elizabeth" sort="Gardiner, Elizabeth" uniqKey="Gardiner E" first="Elizabeth" last="Gardiner">Elizabeth Gardiner</name>
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