PuSH - Publikationsserver des Helmholtz Zentrums München: Monocytes, neutrophils, and platelets cooperate to initiate and propagate venous thrombosis in mice <em>in vivo</em>.

Informationen

Hinweise zu Qualitätskriterien von Zeitschriften

Open-Access-Richtlinie der Helmholtz-Gemeinschaft 2016

CC Licencences

Metriken für Publikationen

Navigation

Startseite

English

Recherche

Erweiterte Suche

Durchblättern nach ...

... HMGU-Autoren/Konsortien

... Organisationsstruktur

... Zeitschriften

... Publikationstypen

... Forschungsdaten

... Arbeitsgruppen

... Erscheinungsjahr

Publikationen im Überblick

Statistik

HGF Fortschrittsbericht

OA Publikationen

Eintragen

Neue Publikation eintragen

Neue Publikation holen aus...

...EVA

Fehlende Publikation melden

Highlights

Suche

Hilfe & Kontakt

Ansprechpartner

Hilfe

Datenschutz

Helmholtz Open Science

Bibliometrische Indikatoren

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

von Brühl, M.L.* ; Stark, K.* ; Steinhart, A.* ; Chandraratne, S.* ; Konrad, I.* ; Lorenz, M.* ; Khandoga, A.* ; Tirniceriu, A.* ; Coletti, R.* ; Köllnberger, M.* ; Byrne, R.A.* ; Laitinen, I.* ; Walch, A.K. ; Brill, A.* ; Pfeiler, S.* ; Manukyan, D.* ; Braun, S.* ; Lange, P.* ; Riegger, J.* ; Ware, J.* ; Eckart, A.* ; Haidari, S.* ; Rudelius, M.* ; Schulz, C.* ; Echtler, K.* ; Brinkmann, V.* ; Schwaiger, M.* ; Preissner, K.T.* ; Wagner, D.D.* ; Mackman, N.* ; Engelmann, B.* ; Massberg, S.*

Monocytes, neutrophils, and platelets cooperate to initiate and propagate venous thrombosis in mice in vivo.

J. Exp. Med. 209, 819-835 (2012)

Verlagsversion Volltext

DOI

PMC

	Closed

Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.

Abstract
Metriken
Zusatzinfos

Deep vein thrombosis (DVT) is a major cause of cardiovascular death. The sequence of events that promote DVT remains obscure, largely as a result of the lack of an appropriate rodent model. We describe a novel mouse model of DVT which reproduces a frequent trigger and resembles the time course, histological features, and clinical presentation of DVT in humans. We demonstrate by intravital two-photon and epifluorescence microscopy that blood monocytes and neutrophils crawling along and adhering to the venous endothelium provide the initiating stimulus for DVT development. Using conditional mutants and bone marrow chimeras, we show that intravascular activation of the extrinsic pathway of coagulation via tissue factor (TF) derived from myeloid leukocytes causes the extensive intraluminal fibrin formation characteristic of DVT. We demonstrate that thrombus-resident neutrophils are indispensable for subsequent DVT propagation by binding factor XII (FXII) and by supporting its activation through the release of neutrophil extracellular traps (NETs). Correspondingly, neutropenia, genetic ablation of FXII, or disintegration of NETs each confers protection against DVT amplification. Platelets associate with innate immune cells via glycoprotein Ibα and contribute to DVT progression by promoting leukocyte recruitment and stimulating neutrophil-dependent coagulation. Hence, we identified a cross talk between monocytes, neutrophils, and platelets responsible for the initiation and amplification of DVT and for inducing its unique clinical features.

Impact Factor

Scopus SNIP

Web of Science
Times Cited

Scopus
Cited By

Altmetric

13.853

2.910

993

1059