Hypercoagulability Inhibits Monocyte Transendothelial Migration Through Protease-Activated Receptor-1-, Phospholipase-Cβ-, Phosphoinositide 3-Kinase-, and Nitric Oxide-Dependent Signaling in Monocytes and Promotes Plaque Stability | Zendy

Stefanie Seehaus | Zendy; Khurrum Shahzad | Zendy; Muhammed Kashif | Zendy; Ilya A. Vinnikov | Zendy; Martin Schiller | Zendy; Hongjie Wang | Zendy; Thati Madhusudhan | Zendy; Volker Eckstein | Zendy; Angelika Bierhaus | Zendy; Florian Bea | Zendy; Erwin Blessing | Zendy; Hartmut Weiler | Zendy; David Frommhold | Zendy; Peter P. Nawroth | Zendy; Berend Isermann | Zendy

Open Access

Hypercoagulability Inhibits Monocyte Transendothelial Migration Through Protease-Activated Receptor-1-, Phospholipase-Cβ-, Phosphoinositide 3-Kinase-, and Nitric Oxide-Dependent Signaling in Monocytes and Promotes Plaque Stability

Author(s) -

Stefanie Seehaus,

Khurrum Shahzad,

Muhammed Kashif,

Ilya A. Vinnikov,

Martin Schiller,

Hongjie Wang,

Thati Madhusudhan,

Volker Eckstein,

Angelika Bierhaus,

Florian Bea,

Erwin Blessing,

Hartmut Weiler,

David Frommhold,

Peter P. Nawroth,

Berend Isermann

Publication year - 2009

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.109.849539

Subject(s) - thrombin , medicine , monocyte , nitric oxide , tissue factor , phospholipase a2 , phospholipase c , thrombomodulin , microbiology and biotechnology , inflammation , receptor , immunology , biology , coagulation , platelet , biochemistry , enzyme

Clinical studies failed to provide clear evidence for a proatherogenic role of hypercoagulability. This is in contrast to the well-established detrimental role of hypercoagulability and thrombin during acute atherosclerotic complications. These seemingly opposing data suggest that hypercoagulability might exert both proatherogenic and antiatherogenic effects. We therefore investigated whether hypercoagulability mediates a beneficial effect during de novo atherogenesis.

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