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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, RESULTS. Meshes: ADAM Proteins, ADAM17 Protein, Animals, Binding Sites, Blood Platelets, Carotid Arteries, Carotid Artery Injuries, Cell Adhesion, Disease Models, Animal, I-kappa B Kinase, Leukocytes, Macrophage-1 Antigen, Mice, Mice, Inbred C57BL, Mice, Knockout, Neointima, Platelet Adhesiveness, Platelet Aggregation, Platelet Glycoprotein GPIb-IX Complex, Protein Binding, Receptors, LDL, Time Factors, Vascular System Injuries.
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Does platelet IκB kinase-β deficiency increase mouse arterial neointima formation via delayed glycoprotein Ibα shedding? Context: 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-β (IKKβ) (IKKβ(fl/fl)/PF4(cre)/LDLR(-/-)) and in control mice (IKKβ(fl/fl)/LDLR(-/-)). The size of the arterial neointima was 61% larger in the IKKβ(fl/fl)/PF4(cre)/LDLR(-/-) mice compared with the littermate control IKKβ(fl/fl)/LDLR(-/-) mice. Compared with the control mice, the IKKβ(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 IKKβ-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 IKKβ-deficient platelets.
assistant
Platelet IKKβ 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. Final Decision: yes