Impaired fibrinolysis in JAK2V617F-related myeloproliferative neoplasms.

JAK2V617F mutation fibrin clot fibrinolysis myeloproliferative neoplasms

Journal

Journal of thrombosis and haemostasis : JTH
ISSN: 1538-7836
Titre abrégé: J Thromb Haemost
Pays: England
ID NLM: 101170508

Informations de publication

Date de publication:
09 Sep 2024
Historique:
received: 06 03 2024
revised: 30 07 2024
accepted: 30 07 2024
medline: 12 9 2024
pubmed: 12 9 2024
entrez: 11 9 2024
Statut: aheadofprint

Résumé

Myeloproliferative neoplasms (MPN) are characterized by a high rate of thrombotic complications that contribute to morbi-mortality. MPN-related thrombogenesis is assumed to be multifactorial involving both pro-coagulant and pro-inflammatory processes. Whether impaired fibrinolysis also participates in the pro-thrombotic phenotype of MPN has been poorly investigated. We determined whether MPN, particularly JAK2V617F-positive MPN, are associated with fibrinolytic changes. Tissue plasminogen activator (tPA)-mediated fibrinolysis was evaluated both in whole blood (WB) and plasma from mice with a hematopoietic-restricted Jak2 In WB from Jak2 Our results suggest that impaired tPA-mediated fibrinolysis represents an important pro-thrombotic mechanism in MPN patients that requires confirmation on larger studies.

Sections du résumé

BACKGROUND BACKGROUND
Myeloproliferative neoplasms (MPN) are characterized by a high rate of thrombotic complications that contribute to morbi-mortality. MPN-related thrombogenesis is assumed to be multifactorial involving both pro-coagulant and pro-inflammatory processes. Whether impaired fibrinolysis also participates in the pro-thrombotic phenotype of MPN has been poorly investigated.
OBJECTIVES OBJECTIVE
We determined whether MPN, particularly JAK2V617F-positive MPN, are associated with fibrinolytic changes.
PATIENTS METHODS
Tissue plasminogen activator (tPA)-mediated fibrinolysis was evaluated both in whole blood (WB) and plasma from mice with a hematopoietic-restricted Jak2
RESULTS RESULTS
In WB from Jak2
CONCLUSIONS CONCLUSIONS
Our results suggest that impaired tPA-mediated fibrinolysis represents an important pro-thrombotic mechanism in MPN patients that requires confirmation on larger studies.

Identifiants

pubmed: 39260744
pii: S1538-7836(24)00487-2
doi: 10.1016/j.jtha.2024.07.031
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Auteurs

Marie-Charlotte Bourrienne (MC)

Unité INSERM U1144, Optimisation Thérapeutique en Neuropsychopharmacologie, Paris, France; Laboratoire Hématologie, AP-HP, Hôpital Bichat-Claude Bernard, F-75018 Paris, France. Electronic address: marie-charlotte.bourrienne@inserm.fr.

Stéphane Loyau (S)

Université Paris Cité and Université Sorbonne Paris Nord, INSERM, LVTS, F-75018 Paris, France.

Dorothée Faille (D)

Unité INSERM U1144, Optimisation Thérapeutique en Neuropsychopharmacologie, Paris, France; Laboratoire Hématologie, AP-HP, Hôpital Bichat-Claude Bernard, F-75018 Paris, France.

Juliette Gay (J)

Unité INSERM U1144, Optimisation Thérapeutique en Neuropsychopharmacologie, Paris, France; Laboratoire Hématologie, AP-HP, Hôpital Bichat-Claude Bernard, F-75018 Paris, France.

Séléna Akhenak (S)

Université Paris Cité and Université Sorbonne Paris Nord, INSERM, LVTS, F-75018 Paris, France.

Carine Farkh (C)

Unité INSERM U1144, Optimisation Thérapeutique en Neuropsychopharmacologie, Paris, France; Laboratoire Hématologie, AP-HP, Hôpital Bichat-Claude Bernard, F-75018 Paris, France.

Véronique Ollivier (V)

Unité INSERM U1144, Optimisation Thérapeutique en Neuropsychopharmacologie, Paris, France.

Mialitiana Solonomenjanahary (M)

Unité INSERM U1144, Optimisation Thérapeutique en Neuropsychopharmacologie, Paris, France.

Sébastien Dupont (S)

Unité INSERM U1144, Optimisation Thérapeutique en Neuropsychopharmacologie, Paris, France.

Christine Choqueux (C)

Université Paris Cité and Université Sorbonne Paris Nord, INSERM, LVTS, F-75018 Paris, France.

Jean-Luc Villeval (JL)

INSERM U1287, Institut Gustave Roussy, Université Paris-Saclay, F-94800 Villejuif France.

Isabelle Plo (I)

INSERM U1287, Institut Gustave Roussy, Université Paris-Saclay, F-94800 Villejuif France.

Valérie Edmond (V)

INSERM U1287, Institut Gustave Roussy, Université Paris-Saclay, F-94800 Villejuif France.

Benoît Ho-Tin-Noé (B)

Unité INSERM U1144, Optimisation Thérapeutique en Neuropsychopharmacologie, Paris, France.

Nadine Ajzenberg (N)

Unité INSERM U1144, Optimisation Thérapeutique en Neuropsychopharmacologie, Paris, France; Laboratoire Hématologie, AP-HP, Hôpital Bichat-Claude Bernard, F-75018 Paris, France.

Mikaël Mazighi (M)

Unité INSERM U1144, Optimisation Thérapeutique en Neuropsychopharmacologie, Paris, France; Département de Neurologie, AP-HP, Hôpital Lariboisière, FHU NeuroVasc, F-75010 Paris, France.

Classifications MeSH