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Aging and the loss of functional reserve capacity is an intrinsic feature of life driven by various factors including genetics, lifestyle, and nutrition. Nutrient signaling has been shown to modulate the onset, progression, and/or delay of many age-associated diseases including cardiovascular disease and neurodegenerative decline. While glycemic and lipid flux have been linked to the premature appearance of in vitro biomarkers of aging, the role of trace metals in age-associated cellular changes remain less clear. The trace metal Selenium (Se) is an essential trace mineral that supports many bodily processes including free radical scavenging, thyroid function, and maintenance of cognitive ability. Our research focused on the potential cellular changes in Human Umbilical Vascular Endothelial Cells (HUVECs) in response to Se deprivation. Exposed to a 48-hour continuous reduced Se exposure, we observed a reduced f-actin protein and gene expression. Interestingly, we observed a compensatory increase in the intermediate filament vimentin, which suggest that Se may have an important role in cytoskeletal maintenance and rearrangement. Keywords: Selenium; Endothelial; Oxidative stress; Vimentin; Actin; Nutrients; Aging