Nancy J. Bigley, Ph.D. (Advisor); Dawn P. Wooley, Ph.D. (Committee Member); Lucile E. Wrenshall, M.D., Ph.D. (Committee Member); Marjorie M. Markopoulos, Ph.D. (Committee Member)
Master of Science (MS)
Endothelial cells are distinct multifunctional cells with essential metabolic and synthetic roles along with their ability to function as selective permeability barrier. Endothelial cells (ECs), the major component of blood vessels, essentially interact directly yet differently with inflammatory cytokines. ECs are well recognized to be polarized cells, but little is known about the potential function of inflammatory mediators. Covid 19 may have long-term health effects on par with chronic illnesses. Vascular inflammatory disease and coagulopathy linked to COVID-19 are exacerbated by endothelial cell (EC) dysfunction. SARS-CoV-2 enters the host cell through the Angiotensin Converting Enzyme 2 (ACE2) receptor and primes the S protein using the serine protease Transmembrane Protease, Serine 2 (TMPRSS2). NRP1 (neuropilin-1) serves as a coreceptor. To deepen comprehension of the role of the cytokines on SARS CoV2 receptors of mouse Hemangioendothelioma endothelial cells is the goal of this research. In order to simulate an anti-inflammatory and pro-inflammatory microenvironment, ECs were treated with the cytokines IL-4 and IFNγ respectively. Immunofluorescence staining for ACE2, NRP1 and TMPRSS2 were then analyzed on the cytokine treated cells. The results indicate an increase in the expression of NRP1 and TMPRSS2 receptors when stimulated with Type I (IFNγ) cytokine (p<0.03) whereas Type II (IL4) induced an enhancement of the ACE2 and TMPRSS2 (p<0.0.3) receptor expression. These findings identify distinct variations in the response of the cell receptors to cytokine stimulation by EOMA cells.
Department or Program
Microbiology and Immunology
Year Degree Awarded
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