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student research day - Case Western Reserve University School of ...

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Stephanie Michal<br />

Establishing if accelerated atherosclerosis mediated by periodontal disease is<br />

attributed to CD36<br />

Stephanie Michal, Maria Febbario<br />

Cell Biology Department<br />

The Cleveland Clinic Lerner Institute<br />

CD36 is an integral membrane glycoprotein found on the surface <strong>of</strong> many cell types and its functions include<br />

recognition <strong>of</strong> apoptotic cells and modified lipids, uptake <strong>of</strong> fatty acids, regulation <strong>of</strong> angiogenesis and recognition<br />

<strong>of</strong> ligands that trigger an innate immune response. This summer, I work in Dr. Maria Febbraio’s laboratory working<br />

on establishing a link between the expression <strong>of</strong> CD36 and the development <strong>of</strong> atherosclerosis. The scavenger<br />

receptor CD36 has been linked to a pro-thrombotic phenotype that is observed in metabolic states marked by<br />

hyperlipidemia. Yet, when a CD36 knockout mouse is created there appears to be no difference between the<br />

knockout and the wild type mice in the development <strong>of</strong> atherosclerosis. From these findings it has been<br />

hypothesized that increasing the inflammatory stimulus that is associated with the generation <strong>of</strong> reactive oxygen<br />

spices that causes oxidant stress is essential for the creation <strong>of</strong> CD36 specific pro-atherogenic ligands. It has<br />

previously been proposed that there is a link between periodontal disease and atherosclerosis because periodontal<br />

disease in some patients represents a state <strong>of</strong> chronic inflammation. The objective <strong>of</strong> the experiment this summer<br />

was to determine if the atherosclerosis that is arbitrated to periodontal disease is CD36 dependent. In order to<br />

perform the experiment I harvested macrophages from the peritoneum <strong>of</strong> both wild type and CD36 knockout mice<br />

and plated the cells. Then four groups were formed, two wild type one with the bacteria in the media and one<br />

without and two knockouts one with bacteria in the media and one without. After 24 hours the media was removed<br />

and the macrophages were stained with oil red O (stains LDL) and fixed. The number <strong>of</strong> foam cells were then<br />

counted using a light microscope. The expected results were that the most foam cells would be found on the plate<br />

<strong>of</strong> wild type macrophages that contained media filled with bacteria however there was no statistical difference<br />

between the plates. In conclusion, I would like to acknowledge the support I received to work on this project from<br />

the T35 grant from the NIH.<br />

59

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