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Platelet IκB kinase-ß deficiency increases mouse arterial neointima formation via delayed glycoprotein Ibα shedding.

Wei, Shujian; Wang, Huan; Zhang, Guoying; Lu, Ying; An, Xiaofei; Ren, Shumei; Wang, Yunmei; Chen, Yuguo; White, James G; Zhang, Chunxiang; Simon, Daniel I; Wu, Chaodong; Li, Zhenyu; Huo, Yuqing.
Arterioscler Thromb Vasc Biol; 33(2): 241-8, 2013 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-23241410


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.


We performed carotid artery wire injuries in low-density lipoprotein receptor-deficient (LDLR(-/-)) mice with a platelet-specific deletion of IκB kinase-ß (IKKß) (IKKß(fl/fl)/PF4(cre)/LDLR(-/-)) and in control mice (IKKß(fl/fl)/LDLR(-/-)). The size of the arterial neointima was 61% larger in the IKKß(fl/fl)/PF4(cre)/LDLR(-/-) mice compared with the littermate control IKKß(fl/fl)/LDLR(-/-) mice. Compared with the control mice, the IKKß(fl/fl)/PF4(cre)/LDLR(-/-) mice exhibited more leukocyte adhesion at the injured area. The extent of glycoprotein Ibα shedding after platelet activation was compromised in the IKKß-deficient platelets. This effect was associated with a low level of the active form of A Disintegrin And Metalloproteinase 17, the key enzyme involved in mediating glycoprotein Ibα shedding in activated IKKß-deficient platelets.


Platelet IKKß deficiency increases the formation of injury-induced arterial neointima formation. Thus, nuclear factor-κB-related inhibitors should be carefully evaluated for use in patients after an arterial intervention.
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