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Platelet I?B kinase-? deficiency increases mouse arterial neointima formation via delayed glycoprotein Ib? shedding.

ABSTRACT: 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-?B is a critical molecule in platelet activation. Here, we investigated the role of the platelet nuclear factor-?B 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 I?B kinase-? (IKK?) (IKK?(fl/fl)/PF4(cre)/LDLR(-/-)) and in control mice (IKK?(fl/fl)/LDLR(-/-)). The size of the arterial neointima was 61% larger in the IKK?(fl/fl)/PF4(cre)/LDLR(-/-) mice compared with the littermate control IKK?(fl/fl)/LDLR(-/-) mice. Compared with the control mice, the IKK?(fl/fl)/PF4(cre)/LDLR(-/-) mice exhibited more leukocyte adhesion at the injured area. The extent of glycoprotein Ib? shedding after platelet activation was compromised in the IKK?-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 Ib? shedding in activated IKK?-deficient platelets.Platelet IKK? deficiency increases the formation of injury-induced arterial neointima formation. Thus, nuclear factor-?B-related inhibitors should be carefully evaluated for use in patients after an arterial intervention.


PROVIDER: S-EPMC3755353 | BioStudies | 2013-01-01

REPOSITORIES: biostudies

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