Abstract:
:Inflammation and thrombosis occur together in many diseases. The leukocyte integrin Mac-1 (also known as integrin αMβ2, or CD11b/CD18) is crucial for leukocyte recruitment to the endothelium, and Mac-1 engagement of platelet GPIbα is required for injury responses in diverse disease models. However, the role of Mac-1 in thrombosis is undefined. Here we report that mice with Mac-1 deficiency (Mac-1-/-) or mutation of the Mac-1-binding site for GPIbα have delayed thrombosis after carotid artery and cremaster microvascular injury without affecting parameters of haemostasis. Adoptive wild-type leukocyte transfer rescues the thrombosis defect in Mac-1-/- mice, and Mac-1-dependent regulation of the transcription factor Foxp1 contributes to thrombosis as evidenced by delayed thrombosis in mice with monocyte-/macrophage-specific overexpression of Foxp1. Antibody and small-molecule targeting of Mac-1:GPIbα inhibits thrombosis. Our data identify a new pathway of thrombosis involving leukocyte Mac-1 and platelet GPIbα, and suggest that targeting this interaction has anti-thrombotic therapeutic potential with reduced bleeding risk.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Wang Y,Gao H,Shi C,Erhardt PW,Pavlovsky A,A Soloviev D,Bledzka K,Ustinov V,Zhu L,Qin J,Munday AD,Lopez J,Plow E,Simon DIdoi
10.1038/ncomms15559subject
Has Abstractpub_date
2017-05-30 00:00:00pages
15559issn
2041-1723pii
ncomms15559journal_volume
8pub_type
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