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Title: Platelet GPIb and downstream activation by S. sanguis
Authors: Abdulrehman, Ahmed Y.
Supervisor: McNicol, Archibald (Oral Biology)
Examining Committee: Chelikani, Prashen (Oral Biology) Scott, James Elliott (Oral Biology) Hatch, Grant (Pharmacology/Biochemistry & Medical Genetics)
Graduation Date: February 2011
Keywords: platelet
Issue Date: 13-Dec-2010
Abstract: There is increasing evidence suggesting the contribution of bacterial infections in atherothrombotic conditions. Studies have demonstrated that bacteria residing within the oral cavity activate platelets once they enter circulation. S. sanguis 2017-78 is capable of stimulating platelet aggregation in a thromboxane-dependent manner. In the present study, the signaling events associated with S. sanguis have been studied further. S. sanguis 2017-78 caused the phosphorylation of p38 MAP kinase and subsequently cPLA2. The p38 MAP kinase inhibitor, SB203580 inhibited S. sanguis 2017-78-induced platelet aggregation as well as the phosphorylation of both p38 MAP kinase and cPLA2. These data are consistent with cPLA2 as a physiological target of p38. A second component of the study examined the effects of aspirin, a known inhibitor of cyclooxygenase, on these signalling pathways.
Appears in Collection(s):FGS - Electronic Theses & Dissertations (Public)

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