Hemostatic disorders in a JAK2V617F-driven mouse model of myeloproliferative neoplasm.
Identifieur interne : 003538 ( PubMed/Corpus ); précédent : 003537; suivant : 003539Hemostatic disorders in a JAK2V617F-driven mouse model of myeloproliferative neoplasm.
Auteurs : Lamia Lamrani ; Catherine Lacout ; Véronique Ollivier ; Cécile V. Denis ; Elizabeth Gardiner ; Benoit Ho Tin Noe ; William Vainchenker ; Jean-Luc Villeval ; Martine Jandrot-PerrusSource :
- Blood [ 1528-0020 ] ; 2014.
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
Links to Exploration step
pubmed:24951423Le document en format XML
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Denis</name><affiliation><nlm:affiliation>Université Paris-Sud 11, Villejuif, France; INSERM, U770, Le Kremlin-Bicêtre, France; and.</nlm:affiliation></affiliation></author><author><name sortKey="Gardiner, Elizabeth" sort="Gardiner, Elizabeth" uniqKey="Gardiner E" first="Elizabeth" last="Gardiner">Elizabeth Gardiner</name><affiliation><nlm:affiliation>Monash University, Clayton, VIC, Australia.</nlm:affiliation></affiliation></author><author><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><affiliation><nlm:affiliation>INSERM, U1148, Paris, France; Université Paris Denis Diderot 7, Paris, France;</nlm:affiliation></affiliation></author><author><name sortKey="Vainchenker, William" sort="Vainchenker, William" uniqKey="Vainchenker W" first="William" last="Vainchenker">William Vainchenker</name><affiliation><nlm:affiliation>INSERM, U1009, Villejuif, France; Université Paris-Sud 11, Villejuif, France; Institut Gustave Roussy, Villejuif, France;</nlm:affiliation></affiliation></author><author><name sortKey="Villeval, Jean Luc" sort="Villeval, Jean Luc" uniqKey="Villeval J" first="Jean-Luc" last="Villeval">Jean-Luc Villeval</name><affiliation><nlm:affiliation>INSERM, U1009, Villejuif, France; Université Paris-Sud 11, Villejuif, France; Institut Gustave Roussy, Villejuif, France;</nlm:affiliation></affiliation></author><author><name sortKey="Jandrot Perrus, Martine" sort="Jandrot Perrus, Martine" uniqKey="Jandrot Perrus M" first="Martine" last="Jandrot-Perrus">Martine Jandrot-Perrus</name><affiliation><nlm:affiliation>INSERM, U1148, Paris, France; Université Paris Denis Diderot 7, Paris, France;</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24951423</idno><idno type="pmid">24951423</idno><idno type="doi">10.1182/blood-2013-10-530832</idno><idno type="wicri:Area/PubMed/Corpus">003538</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003538</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Hemostatic disorders in a JAK2V617F-driven mouse model of myeloproliferative neoplasm.</title><author><name sortKey="Lamrani, Lamia" sort="Lamrani, Lamia" uniqKey="Lamrani L" first="Lamia" last="Lamrani">Lamia Lamrani</name><affiliation><nlm:affiliation>INSERM, U1148, Paris, France; Université Paris Denis Diderot 7, Paris, France;</nlm:affiliation></affiliation></author><author><name sortKey="Lacout, Catherine" sort="Lacout, Catherine" uniqKey="Lacout C" first="Catherine" last="Lacout">Catherine Lacout</name><affiliation><nlm:affiliation>INSERM, U1009, Villejuif, France; Université Paris-Sud 11, Villejuif, France; Institut Gustave Roussy, Villejuif, France;</nlm:affiliation></affiliation></author><author><name sortKey="Ollivier, Veronique" sort="Ollivier, Veronique" uniqKey="Ollivier V" first="Véronique" last="Ollivier">Véronique Ollivier</name><affiliation><nlm:affiliation>INSERM, U1148, Paris, France; Université Paris Denis Diderot 7, Paris, France;</nlm:affiliation></affiliation></author><author><name sortKey="Denis, Cecile V" sort="Denis, Cecile V" uniqKey="Denis C" first="Cécile V" last="Denis">Cécile V. Denis</name><affiliation><nlm:affiliation>Université Paris-Sud 11, Villejuif, France; INSERM, U770, Le Kremlin-Bicêtre, France; and.</nlm:affiliation></affiliation></author><author><name sortKey="Gardiner, Elizabeth" sort="Gardiner, Elizabeth" uniqKey="Gardiner E" first="Elizabeth" last="Gardiner">Elizabeth Gardiner</name><affiliation><nlm:affiliation>Monash University, Clayton, VIC, Australia.</nlm:affiliation></affiliation></author><author><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><affiliation><nlm:affiliation>INSERM, U1148, Paris, France; Université Paris Denis Diderot 7, Paris, France;</nlm:affiliation></affiliation></author><author><name sortKey="Vainchenker, William" sort="Vainchenker, William" uniqKey="Vainchenker W" first="William" last="Vainchenker">William Vainchenker</name><affiliation><nlm:affiliation>INSERM, U1009, Villejuif, France; Université Paris-Sud 11, Villejuif, France; Institut Gustave Roussy, Villejuif, France;</nlm:affiliation></affiliation></author><author><name sortKey="Villeval, Jean Luc" sort="Villeval, Jean Luc" uniqKey="Villeval J" first="Jean-Luc" last="Villeval">Jean-Luc Villeval</name><affiliation><nlm:affiliation>INSERM, U1009, Villejuif, France; Université Paris-Sud 11, Villejuif, France; Institut Gustave Roussy, Villejuif, France;</nlm:affiliation></affiliation></author><author><name sortKey="Jandrot Perrus, Martine" sort="Jandrot Perrus, Martine" uniqKey="Jandrot Perrus M" first="Martine" last="Jandrot-Perrus">Martine Jandrot-Perrus</name><affiliation><nlm:affiliation>INSERM, U1148, Paris, France; Université Paris Denis Diderot 7, Paris, France;</nlm:affiliation></affiliation></author></analytic><series><title level="j">Blood</title><idno type="eISSN">1528-0020</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Aorta (metabolism)</term><term>Aorta (pathology)</term><term>Aorta (physiopathology)</term><term>Bleeding Time</term><term>Blood Platelets (metabolism)</term><term>Disease Models, Animal</term><term>Flow Cytometry</term><term>Gene Knock-In Techniques</term><term>Hemostatic Disorders (genetics)</term><term>Humans</term><term>Immunoblotting</term><term>Janus Kinase 2 (genetics)</term><term>Mice, Transgenic</term><term>Mutation, Missense</term><term>Myeloproliferative Disorders (blood)</term><term>Myeloproliferative Disorders (genetics)</term><term>Platelet Activation (genetics)</term><term>Platelet Membrane Glycoproteins (genetics)</term><term>Platelet Membrane Glycoproteins (metabolism)</term><term>Polycythemia Vera (blood)</term><term>Polycythemia Vera (genetics)</term><term>Primary Myelofibrosis (blood)</term><term>Primary Myelofibrosis (genetics)</term><term>Thrombosis (blood)</term><term>Thrombosis (genetics)</term><term>Vasodilation (genetics)</term><term>von Willebrand Factor (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Janus Kinase 2</term><term>Platelet Membrane Glycoproteins</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Myeloproliferative Disorders</term><term>Polycythemia Vera</term><term>Primary Myelofibrosis</term><term>Thrombosis</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Hemostatic Disorders</term><term>Myeloproliferative Disorders</term><term>Platelet Activation</term><term>Polycythemia Vera</term><term>Primary Myelofibrosis</term><term>Thrombosis</term><term>Vasodilation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Aorta</term><term>Blood Platelets</term><term>Platelet Membrane Glycoproteins</term><term>von Willebrand Factor</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Aorta</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Aorta</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><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><term>Mice, Transgenic</term><term>Mutation, Missense</term></keywords></textClass></profileDesc></teiHeader><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 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