Platelet IκB Kinase-β Deficiency Increases Mouse Arterial Neointima Formation via Delayed Glycoprotein Ibα Shedding | Zendy

Shujian Wei | Zendy; Huan Wang | Zendy; Guoying Zhang | Zendy; Ying Lu | Zendy; Xiaofei An | Zendy; Shumei Ren | Zendy; Yunmei Wang | Zendy; Yuguo Chen | Zendy; James G. White | Zendy; Chunxiang Zhang | Zendy; Daniel I. Simon | Zendy; Chaodong Wu | Zendy; Zhenyu Li | Zendy; Yuqing Huo | Zendy

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Platelet IκB Kinase-β Deficiency Increases Mouse Arterial Neointima Formation via Delayed Glycoprotein Ibα Shedding

Author(s) -

Shujian Wei,

Huan Wang,

Guoying Zhang,

Ying Lu,

Xiaofei An,

Shumei Ren,

Yunmei Wang,

Yuguo Chen,

James G. White,

Chunxiang Zhang,

Daniel I. Simon,

Chaodong Wu,

Zhenyu Li,

Yuqing Huo

Publication year - 2012

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.112.300781

Subject(s) - neointima , platelet , ldl receptor , platelet activation , platelet membrane glycoprotein , chemistry , medicine , endocrinology , restenosis , biology , lipoprotein , cholesterol , stent

On the luminal surface of injured arteries, platelet activation and leukocyte-platelet interactions are critical for the initiation and progression of arterial restenosis. The transcription factor nuclear factor-κB is a critical molecule in platelet activation. Here, we investigated the role of the platelet nuclear factor-κB pathway in forming arterial neointima after arterial injury.

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