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Full-Text Articles in Life Sciences

Regulation Of In Vitro And In Vivo Hepatic Stellate Cell Activation By The Ayrl Hydrocarbon Receptor, Shivakumar Rayavara Veerabhadraiah Dec 2020

Regulation Of In Vitro And In Vivo Hepatic Stellate Cell Activation By The Ayrl Hydrocarbon Receptor, Shivakumar Rayavara Veerabhadraiah

Boise State University Theses and Dissertations

Liver fibrosis is a pathological condition characterized by the excessive deposition of extracellular matrix material by activated hepatic stellate cells (HSCs). We recently reported that activation of the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increases HSC activation in vitro and in mouse models of experimental liver fibrosis. The goal of this project was to determine the mechanism by which AhR activation impacts HSC activation and the subsequent development of liver fibrosis. It is possible that HSCs are direct cellular targets for TCDD. Alternatively, TCDD could increase HSC activation indirectly by exacerbating hepatocyte damage …


Prevalence Of Anticoagulant Rodenticides In Ferruginous Hawk Nestlings And Evaluation Of A Novel Method To Rapidly Assess Exposure, Ariana Joyce Dickson Aug 2020

Prevalence Of Anticoagulant Rodenticides In Ferruginous Hawk Nestlings And Evaluation Of A Novel Method To Rapidly Assess Exposure, Ariana Joyce Dickson

Boise State University Theses and Dissertations

Anticoagulant rodenticides (ARs) are compounds commonly used to control rodent pests by inhibiting an enzyme critical for synthesis of clotting factors in their blood. Secondary and tertiary poisoning of non-target species frequently occur, especially of predators that consume rodents, including many species of raptors. Although raptor exposure to ARs has been documented on at least three continents, patterns, pathways and the sub-lethal effects of exposure are not well studied. This has created a substantial need to monitor the effects of ARs in free-living populations. I evaluated the prevalence of secondary, non-target exposure to anticoagulant rodenticides experienced by a predatory raptor, …


Acute Exposure To Tcdd Increases Liver Disease Progression In Mice With Carbon Tetrachloride-Induced Liver Injury, Giovan N. Cholico Dec 2019

Acute Exposure To Tcdd Increases Liver Disease Progression In Mice With Carbon Tetrachloride-Induced Liver Injury, Giovan N. Cholico

Boise State University Theses and Dissertations

Liver disease is a worldwide problem and the 9th leading cause of death in the United States. Common causes of liver disease include alcohol abuse, virus infection, and nonalcoholic fatty liver. Regardless of etiology, liver damage elicits inflammation and drives the activation of hepatic stellate cells (HSCs), which deposit collagen throughout the liver. During chronic injury, excessive collagen deposition, referred to as fibrosis or “scarring”, can progress to cirrhosis, cancer, and organ failure. Emerging evidence indicates a strong association between liver disease and exposure to environmental chemicals. This research investigated mechanisms by which exposure to the environmental contaminant 2,3,7,8-tetrachlorodibenzo- …


Consequences Of 2,3,7,8-Tetrachlorodibenzo-P-Dioxin (Tcdd) On Hepatic Stellate Cell Activation And Extracellular Matrix Remodeling During Chronic Liver Injury, Cheri Lou Lamb May 2016

Consequences Of 2,3,7,8-Tetrachlorodibenzo-P-Dioxin (Tcdd) On Hepatic Stellate Cell Activation And Extracellular Matrix Remodeling During Chronic Liver Injury, Cheri Lou Lamb

Boise State University Theses and Dissertations

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental pollutant and high-affinity ligand for the aryl hydrocarbon receptor (AhR). Exposure to TCDD elicits a spectrum of toxic effects, many involving aberrant cell proliferation, activation, and differentiation. The liver is a target organ for TCDD toxicity, and increasing evidence indicates that AhR signaling regulates genes that coordinate deposition and remodeling of the extracellular matrix (ECM) in the liver. Hepatic stellate cells (HSCs) are central to ECM remodeling in the liver. We recently reported that TCDD treatment increases the activation of human HSCs in vitro. The goal of this study was to …


Immunoregulation Of Liver Regeneration By The Aryl Hydrocarbon Receptor: Role Of Lymphocytes And Interferon-Gamma, Christopher John Horras Aug 2011

Immunoregulation Of Liver Regeneration By The Aryl Hydrocarbon Receptor: Role Of Lymphocytes And Interferon-Gamma, Christopher John Horras

Boise State University Theses and Dissertations

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant that elicits toxicity by activating the aryl hydrocarbon receptor. The toxic effects associated with TCDD exposure include immunotoxicity and dysregulated cell cycle control, although the mechanisms are poorly understood. A previous report indicates that exposure to TCDD suppresses hepatocyte proliferation in a mouse model of liver regeneration induced by 70% partial hepatectomy (PH). Based on reports that liver regeneration is negatively regulated by interferon (IFN)-γ produced by activated natural killer (NK) cells, along with the well-established immunotoxic effects of TCDD in other model systems, we hypothesized that TCDD treatment attenuates liver …


Immunomodulatory Effects Of Diesel Exhaust Particles, Ashley Kay Masterson Dec 2009

Immunomodulatory Effects Of Diesel Exhaust Particles, Ashley Kay Masterson

Boise State University Theses and Dissertations

Diesel exhaust particles (DEP) represent a key component of particulate matter pollution and a serious cardiopulmonary health risk, as these particles have been associated with increased morbidity and mortality following exposure. In this study, we investigated the immunomodulatory properties of DEP on helper T cells by measuring changes in activation, cytokine production, and viability. The expression of CD40L, a key regulatory protein, was increased by DEP in the absence of physiologic stimuli without parallel increases in the expression of CD25 and CD69 activation markers. Additional studies utilizing a variety of T cell stimuli, including T cell receptor signaling and CD28 …