College of Agriculture & Natural Resources

Permanent URI for this communityhttp://hdl.handle.net/1903/1598

The collections in this community comprise faculty research works, as well as graduate theses and dissertations.

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Subject: search.filters.subject.apoptosis

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    Interference of Apoptosis by Hepatitis B Virus
    (MDPI, 2017-08-18) Lin, Shaoli; Zhang, Yan-Jin
    Hepatitis B virus (HBV) causes liver diseases that have been a consistent problem for human health, leading to more than one million deaths every year worldwide. A large proportion of hepatocellular carcinoma (HCC) cases across the world are closely associated with chronic HBV infection. Apoptosis is a programmed cell death and is frequently altered in cancer development. HBV infection interferes with the apoptosis signaling to promote HCC progression and viral proliferation. The HBV-mediated alteration of apoptosis is achieved via interference with cellular signaling pathways and regulation of epigenetics. HBV X protein (HBX) plays a major role in the interference of apoptosis. There are conflicting reports on the HBV interference of apoptosis with the majority showing inhibition of and the rest reporting induction of apoptosis. In this review, we described recent studies on the mechanisms of the HBV interference with the apoptosis signaling during the virus infection and provided perspective.
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    Interference of Apoptosis by Hepatitis B Virus
    (MDPI, 2017-08-18) Lin, Shaoli; Zhang, Yan-Jin
    Hepatitis B virus (HBV) causes liver diseases that have been a consistent problem for human health, leading to more than one million deaths every year worldwide. A large proportion of hepatocellular carcinoma (HCC) cases across the world are closely associated with chronic HBV infection. Apoptosis is a programmed cell death and is frequently altered in cancer development. HBV infection interferes with the apoptosis signaling to promote HCC progression and viral proliferation. The HBV-mediated alteration of apoptosis is achieved via interference with cellular signaling pathways and regulation of epigenetics. HBV X protein (HBX) plays a major role in the interference of apoptosis. There are conflicting reports on the HBV interference of apoptosis with the majority showing inhibition of and the rest reporting induction of apoptosis. In this review, we described recent studies on the mechanisms of the HBV interference with the apoptosis signaling during the virus infection and provided perspective.
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    ENERGY METABOLISM IN DEVELOPING CHICKEN LYMPHOCYTES DURING THE EMBRYONIC TO POSTHATCH TRANSITION
    (2007-07-26) Rudrappa, Shashidhara Govindareddy; Porter, Tom E; Humphrey, Brooke D; Animal Sciences; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    In chickens, the primary energy substrate is lipid during embryogenesis and carbohydrate after hatch. Accordingly, chicks adapt their metabolism to utilize glucose after hatch; however, little is known about metabolic adaptation in developing lymphocytes. Therefore, the objective of this dissertation was to examine metabolic adaptation in developing lymphocytes and the associated impact on their development. The first objective examined energy substrate utilization in bursacytes and thymocytes during the embryonic to posthatch transition. Glucose metabolism increased in both lymphocyte populations during the first two weeks posthatch due to increased glucose transporter-3 mRNA abundance, glucose uptake and hexokinase activity. Additionally, some of these metabolic markers were positively correlated with the serum glucose concentration. Glutamine metabolism increased in bursacytes only, and lipid metabolism was unaltered in both populations. Collectively, glucose is a preferred energy substrate for lymphocytes posthatch, and glucose utilization by developing lymphocytes may be related to the serum glucose concentration. The second objective determined the effect of glucose availability on thymocyte metabolism, energy status and survival. Embryonic thymic lobes were grown in culture in media containing varying glucose concentrations. Thymocyte glucose metabolism and mitochondria membrane potential were highest in 15 mM glucose and apoptosis was highest in 5mM glucose. Collectively, glucose availability regulates glucose metabolism in thymocytes, and these changes in glucose metabolism were related to thymocyte energy status and survival. The third objective determined the effect of glucose availability on T cell development. Thymocyte Interleukin-7Rα (IL-7Rα) mRNA abundance and CD4+ T cell numbers over the culture period were dependent upon glucose availability. Between 12 and 24 h, thymocyte IL-7Rα mRNA abundance increased in 5 mM increased 1.74-fold, while it decreased in 15 mM by 58.6%. CD4+ numbers decreased with time in 5 mM, whereas they increased with time in 15 mM. T cell receptor (TCR) β excision circles were higher in 15 mM compared to 5 mM at 12 h. Glucose availability alters TCR β rearrangement, IL-7Rα gene expression and CD4+ T cell development, which may influence naïve T cell generation. As thymocytes develop in a low glucose environment in ovo, this may be one factor that limits T cell development until hatch.