Dual roles for polo-like kinase 3 in the regulation of platelet function

Date
2013
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University of Delaware
Abstract
A consequence of the increase in life expectancy of developed nations is that their citizens become increasingly subject to diseases that may manifest only in the later years of life. Cardiovascular disease (CVD) is one such disease, and it often ranks as the number one killer of the denizens of the Western world. Indeed, the increasing potential for us to live lives that are ever more sedentary means that even the middle-aged have become susceptible to it, under the right conditions. Perhaps it is no surprise then, that much time and effort has been spent in the past several decades to find the causes and potential treatments for this disease. Despite this, our understanding of the inner workings of the platelet, a cell of the blood and prime participant in the pathology of CVD, is still surprisingly limited. Polo-like kinase 3 (Plk3) is a protein that may be key to these inner workings. My research has identified a novel role for Polo-like kinase 3 in controlling platelet function. This protein appears to not only affect the activity of the integrin aIIbß3, but also to assist in the process of granular secretion. Using a mouse model in which the Plk3 gene was ablated, I established that Plk3 -/-platelets exhibit hyperaggregation compared to WT platelets. They also bind fibrinogen more effectively and will adhere to a fibrinogen coated surface to a greater extent than WT platelets. Conversely, granular secretion is reduced in Plk3 -/-platelets when stimulated with thrombin. Taken together, these results indicate that the Plk3 protein plays a dual role in regulating platelet function.
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