Browsing by Subject "Department of Biomedical Sciences"

Now showing 1 - 4 of 4
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    Effects of oxygen availability on metabolic enzyme abundances in Leptomonas pyrrhocoris
    (2024-04-26) Tangen, Madelyn R
    Trypanosomes are parasitic protozoans. Trypanosomes have a unique membrane-bound metabolic organelle called the glycosome, which contains the first seven steps of glycolysis. It is thought the glycosome formed to facilitate enzymatic overhauls that were cellular responses to altered environmental conditions. Environmental changes are more apparent for dual-host trypanosomes, but the glycosome is still found in single-host species. This led to the research question: In single-host trypanosomes, what environmental condition could potentially cause glycosomal protein abundance changes? We hypothesized that a dramatic change in oxygen levels is responsible for the overhaul of glycosomal enzymes in the single-host trypanosome species Leptomonas pyrrhocoris. Additionally, this overhaul would not be seen in metabolic enzymes located outside the glycosome. To test the hypothesis, Leptomonas pyrrhocoris cells were placed in hypoxia and normoxia conditions. Cell counting and protein collection occurred on days two, three, and six. The abundances of five glycosomal enzymes and one cytoplasmic enzyme were measured via western blotting. Significance was determined through an unpaired two-tailed t-test. Trends observed in all enzymes showed that by day three enzymatic abundance was greater in hypoxia. This trend was either maintained or amplified through day six in all but one enzyme. However, because this trend was also observed in the cytosolic enzyme, the hypothesis was rejected. The trend seen in all enzymes suggests that while a change in oxygen level does cause an enzymatic overhaul, it is not one related to the glycosome.
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    Immune Cell Changes in Pancreatic Islets in Offspring of Hypertensive Pregnancies
    (2020) Towner, Kendra; Root, Kate; Hamm, Cassandra M; Regal, Jean
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    Role of Innate Immune Macrophages in Pregnancy-Induced Hypertension
    (2020-04) Hamm, Cassandra M; Towner, Kendra; Root, Kate; Regal, Jean
    Preeclampsia is a pregnancy-specific disease characterized by abnormal arterial remodeling that results in placental insufficiency and placental ischemia. Recent studies have shown a specific association with macrophages and the development of hypertension. Macrophages are large, phagocytic white blood cells that have the ability to attack foreign cells and unhealthy self-cells. The pro-inflammatory cytokines produced by macrophages have been shown to contribute to blood pressure elevation and subsequent tissue damage. Macrophages can further polarize into different subtypes, labelled as M1 and M2 macrophages. In preeclampsia, data suggests that M1 macrophages increase at the maternal-fetal interface. Normally numerous macrophages reside in the peritoneal cavity and can move to different sites throughout the body depending on the circumstances. We hypothesized that placental ischemia results in macrophage movement from the peritoneal cavity to the site of ischemia in the placenta.
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    The Role of Macrophages in Developmental Programming of Type 2 Diabetes
    (2021-03-15) Molin, Alexa M; Root, Kate; Polack, Vonda; Huchthausen, Margaretta; Regal, Jean
    Hypertensive disorders are a common pregnancy complication that can increase the risk of developing type 2 diabetes (T2D) in offspring. Preeclampsia, a hypertensive disorder characterized by high blood pressure with new-onset proteinuria is initiated by placental ischemia. Studies from the Regal lab showed placental ischemia induced hypertension in female rat offspring leads to a reduced β-cell area associated with an increase in pancreatic islet macrophages. Therefore, depletion of macrophages may allow beta-cell area to recover and lower the risk of T2D. The goal of this study is to deplete macrophages in the pancreatic islets using Clophosome clodronate injections of postnatal day 13 female rats.