MU-COM Research Day
User Collection Publique
262 Article
Actions
Last Updated: 2021-10-22
Détails de la collection
MU-COM Research Day is an annual showcase of the the research engagement of the students within the College of Osteopathic Medicine. Content on display are typically poster presentations along with faculty-led discussions of research projects. This event is coordinated by the MU-COM Research Club as well as the Faculty-led Research Club Committee.- Articles au total
-
265
Collections parentales (1)
Travaux (262)
211. The Role of CaMKK2 in Whole-Body Metabolism and Bone Remodeling
- Title Tesim:
- The Role of CaMKK2 in Whole-Body Metabolism and Bone Remodeling
- Créateur:
- Sankar, Uma, Patel, Sheel, and Williams, Justin
- Related Url Tesim:
- Audio presentation: https://marian.hosted.panopto.com/Panopto/Pages/Viewer.aspx?id=b81475e6-84cb-4614-bb8b-adf70123880d
- La description:
- Obesity and metabolic dysfunction negatively impacts many tissues, including the skeleton. Calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) is a serine/threonine protein kinase and key regulator of whole-body energy homeostasis. Previous studies have shown that male Camkk2-/- mice are protected from high-fat diet induced obesity, glucose intolerance and insulin resistance. CaMKK2 regulates hypothalamic control of appetite, hepatic gluconeogenesis, and insulin production by pancreatic β cells. Deletion of CaMKK2 has also been shown to enhance bone mass and strength in mice. The skeleton is recognized as a highly dynamic and metabolic tissue capable of regulating systemic glucose metabolism. The role of CaMKK2 in bone-mediate regulation of whole-body metabolism is unknown.
- Declaração de direitos:
- http://rightsstatements.org/vocab/InC/1.0/
- La langue:
- English
- Type:
- Poster
- Mot-clé:
- Obesity, metabolic dysfunction, Whole-Body Metabolism, Bone Remodeling, and CaMKK2
- date créée:
- 2021
212. The Role of CBX5 in Head and Neck Cancer Cell Phenotypic Expression
- Title Tesim:
- The Role of CBX5 in Head and Neck Cancer Cell Phenotypic Expression
- Créateur:
- Doci, Colleen, Zemkewicz, John, and Main, Kegan
- Related Url Tesim:
- Audio presentation: https://marian.hosted.panopto.com/Panopto/Pages/Viewer.aspx?id=3daaeda9-1be5-4feb-83ad-ac7300027094
- La description:
- Head and neck squamous cell carcinomas (HNSCCs) have remained one of the common and lethal cancers around the world. HNSCC rapidly spread via the lymphatics system, leading to a higher percentage of initial late-stage diagnoses and poor prognoses for patients. CBX5 is downregulated highly metastatic breast cancers and may repress metastatic phenotypes. It is unclear what role is may have in HNSCC, or which specific functions of CBXS drive its antimetastatic role. We aim to map molecular changes to phenolypic expression in order to provide better diagnostic prognoses for different HNSCC cell types as well as possible pharmacologic targets for treatment.
- Declaração de direitos:
- http://rightsstatements.org/vocab/InC/1.0/
- La langue:
- English
- Type:
- Poster
- Mot-clé:
- CBX5 and Head and neck squamous cell carcinomas (HNSCCs)
- date créée:
- 2020
213. The Role of CBX5 in Head and Neck Cancer Cell Phenotypic Expression
- Title Tesim:
- The Role of CBX5 in Head and Neck Cancer Cell Phenotypic Expression
- Créateur:
- Doci, Colleen, Zemkewicz, John, and Main, Kegan
- La description:
- •Head and neck squamous cell carcinomas (HNSCCs) have remained one of the common and lethal cancers around the world. •HNSCC rapidly spread via the lymphatics system, leading to a higher percentage of initial late-stage diagnoses and poor prognoses for patients. •CBX5 is downregulated highly metastatic breast cancers and may repress metastatic phenotypes •It is unclear what role is may have in HNSCC, or which specific functions of CBX5 drive its antimetastatic role. •We aim to map molecular changes to phenotypic expression in order to provide better diagnostic prognoses for different HNSCC cell types as well as possible pharmacologic targets for treatment.
- Declaração de direitos:
- http://rightsstatements.org/vocab/InC/1.0/
- La langue:
- English
- Type:
- poster
- date créée:
- 1/1/2020
214. Role of cyclooxygenase inhibitors in blocking Coxiella burnetii intracellular growth
- Title Tesim:
- Role of cyclooxygenase inhibitors in blocking Coxiella burnetii intracellular growth
- Créateur:
- Mulye, Minal, Kim, Constantine, Shain, Michael, Harrison, Morgan, and Wooten, Steven
- La description:
- Coxiella burnetii is an obligate intracellular bacterial pathogen and a causative agent of culture-negative endocarditis. While Coxiella initially infects alveolar macrophages, it may disseminate and cause endocarditis up to 20 years after initial infection, which can be fatal if untreated. Even for those receiving treatment, the mortality rate is 19%. Further the treatment has several restrictions and poses significant side effects. Hence, designing better treatments is crucial. To this end, it is important to determine the pathogenesis of Coxiella endocarditis. The occurrence of Coxiella endocarditis several years after initial infection suggests that the bacterium survives long term by subverting host immune response. Our overall goal is to elucidate the specific host immune pathways Coxiella modulates to achieve long-term intracellular survival and identify potential therapeutic targets. Previous studies in endocarditis patients demonstrated an increase in lipid immune mediator prostaglandin E2 (PGE2) which contributed to immunosuppression and promoted bacterial growth suggesting PGE2 importance in Coxiella survival. Our preliminary ELISAs in Coxiella-infected mouse alveolar macrophages demonstrated increased PGE2 production. Since PGE2 production directly correlates to the enzyme cyclooxygenase (Cox) expression and activity, we determined expression of constitutive Cox-1 and inducible Cox-2 genes. Compared to uninfected cells, our gene expression analysis revealed Cox-2 but not Cox-1 upregulation in Coxiellainfected alveolar macrophages. Hence, we hypothesize that inhibition of Cox-2 activity blocks Coxiella intracellular growth. To test this, we are currently treating Coxiellainfected cells with FDA-approved Cox-2 inhibitor celecoxib and pan-Cox inhibitor aspirin. Compared to untreated cells, our preliminary qualitative microscopic analysis suggests Coxiella growth inhibition in celecoxib and aspirin-treated cells. Ongoing studies are quantifying changes in Coxiella growth after celecoxib and aspirin treatment. Future studies will elucidate the mechanisms Coxiella employs to regulate Cox-2 expression and PGE2 production to induce immunosuppression.
- Declaração de direitos:
- http://rightsstatements.org/vocab/InC/1.0/
- La langue:
- English
- Type:
- presentation
- date créée:
- 11/22/2019
215. The Role of GM-CSF in the Neuropathogenesis of Simian Immunodeficiency Virus (SIV)
- Title Tesim:
- The Role of GM-CSF in the Neuropathogenesis of Simian Immunodeficiency Virus (SIV)
- Créateur:
- Meckley, Rachael and Delery, Elizabeth
- Related Url Tesim:
- Audio presentation: https://marian.hosted.panopto.com/Panopto/Pages/Viewer.aspx?id=6ec5d908-de34-4833-8ac2-adf701234649
- La description:
- Why do neurocognitive disorders persist in people living with HIV while taking combination antiretroviral therapy (cART)? • The brain is a known reservoir for HIV. • HIV can act on myeloid cell populations like macrophages. • Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) is a hematopoietic growth factor and type I soluble cytokine that has been demonstrated to have a proinflammatory role over macrophages (and other myeloid cells) and can induce proliferation and migration across the blood brain barrier (Vogel 2015). • GM-CSF has also been found to be present and is involved in the inflammation process of Simian Immunodeficiency Virus (SIV). • Along with GM-CSF, the expression of GM-CSF receptors has been shown to be increased in SIV. Hypothesis: In SIV infected regions of the midbrain, GM-CSF expression will be increased, which would contribute to the HIV neuropathogenesis by attracting inflammatory cells such as macrophages.
- Declaração de direitos:
- http://rightsstatements.org/vocab/InC/1.0/
- La langue:
- English
- Type:
- Poster
- Mot-clé:
- HIV, neurocognitive disorders, and Simian Immunodeficiency Virus
- date créée:
- 2021
216. The Role of Lipid Droplets in Host-pathogen Interactions of Intracellular and Extracellular Bacteria
- Title Tesim:
- The Role of Lipid Droplets in Host-pathogen Interactions of Intracellular and Extracellular Bacteria
- Créateur:
- Mulye, Minal, Ahila, Ahila, and McDevitt, Adam
- La description:
- Context: Lipid droplets (LDs) are cytoplasmic lipid storage organelles that have recently gained importance in host-pathogen interactions. They are surrounded by a phospholipid monolayer and store excess cellular free fatty acids and cholesterol as triacylglycerol (TAG) and cholesterol ester (CE) respectively. LDs are crucial to lipid metabolism and energy homeostasis. Further, their role in membrane trafficking, cell signaling, and inflammation make them a prime target for pathogens. Several bacterial, viral, and protozoal pathogens exploit host- or self-derived LDs to build new infectious progeny and/or modulate inflammation to promote infection. However, the diverse role of LDs in different bacterial pathogens remains elusive and merits in-depth elucidation. Objective: The goal of this review is to summarize the current research describing how certain bacterial pathogens manipulate LDs, and how those LDs affect the survival and infectivity of said bacteria. Methods/Design: We investigated literature from the last ten years involving LD-pathogen interactions for the intracellular pathogens Mycobacterium tuberculosis, Mycobacterium leprae, and Mycobacterium bovis; and the extracellular pathogens Pseudomonas aeruginosa and Vibrio cholera. Results: Mycobacterium spp. use LDs as both a fatty acid reservoir and a source of immune mediators, thus enhancing bacterial growth. Pseudomonas mobilizes LDs to increase its virulence whereas V. cholera uses fatty acids derived from aquatic animals to remodel its membrane phospholipids and provide stability for the bacterium. Conclusion: Because LDs are important metabolic organelles, understanding how pathogens exploit LDs during infection will emphasize the underappreciated role of cellular metabolic processes during bacterial infections. Our review will shed light on the importance of LDs during intracellular and extracellular bacterial infections, exploring a novel aspect of host-pathogen interactions.
- Declaração de direitos:
- http://rightsstatements.org/vocab/InC/1.0/
- La langue:
- English
- Type:
- poster
- date créée:
- 11/9/2018
217. Role of Lipid Droplets in Prostaglandin E2 Production During Coxiella Burnetii Infection
- Title Tesim:
- Role of Lipid Droplets in Prostaglandin E2 Production During Coxiella Burnetii Infection
- Créateur:
- Mulye, Minal and Harrison, Morgan
- La description:
- Coxiella burnetii is an obligate intracellular bacterial pathogen and causative agent of Q fever. Chronic Q-fever manifests as potentially fatal endocarditis weeks to years after initial infection, suggesting Coxiella’s ability to live long-term inside the host. Our overall goal is to understand Coxiella’s long-term survival mechanisms. While Coxiella initially infects alveolar macrophages, it's also found in lipid droplet (LD)-containing foamy macrophages in cardiac valves of endocarditis patients. Our previous studies show Coxiella manipulates LD homeostasis via the Type 4 Secretion System (T4SS), a major virulence factor which secretes bacterial effector proteins into the host cell cytoplasm to manipulate cell processes. Further, inhibiting LD breakdown almost completely blocks bacterial growth. Since LD breakdown releases lipids, our data suggests LD-derived lipids are critical for Coxiella survival. LD breakdown releases arachidonic acid, a precursor of prostaglandin E2 (PGE2), which promotes an immunosuppressive environment in alveolar macrophages. Hence we hypothesize Coxiella achieves long-term intracellular survival by manipulating host cell LD metabolism to establish a PGE2-mediated immunosuppressive environment. To test this hypothesis, we quantified gene expression of PGE2 synthesis enzyme cyclooxygenase-2 (cox-2) in differentially infected alveolar macrophages. Compared to uninfected cells, cox-2 was upregulated in Coxiella-infected macrophages but not T4SS mutant-infected cells. Further, quantitation by ELISA showed increased PGE2 levels in Coxiella-infected cells compared to uninfected cells. These studies indicate Coxiella T4SS actively manipulates cox-2 expression thus resulting in increased PGE2 in Coxiella-infected cells. Ongoing studies are identifying the direct correlation between LDs and PGE2 production in Coxiella-infected cells. Future studies will determine the potential of blocking PGE2 as a supplemental therapy for Coxiella endocarditis.
- Declaração de direitos:
- http://rightsstatements.org/vocab/InC/1.0/
- La langue:
- English
- Type:
- poster
- date créée:
- 11/9/2018
218. The Role of Notum in Bone’s Response to Mechanical Loading and Aging
- Title Tesim:
- The Role of Notum in Bone’s Response to Mechanical Loading and Aging
- Créateur:
- Hum, Julia, Marshall, Vince, and Wacker, Bryan
- La description:
- Osteoporosis is a silent, dangerous, pathology frequently undiagnosed until patients experience a major fracture. Fractures from osteoporosis lead to a 20% increase of mortality, revealing a need for novel anabolic therapies. Recently, mice lacking Notum protein expression were reported to have increased endocortical bone formation and strength. Notum is an inhibitory protein of the Wnt pathway, a major growth pathway in mammalians. The hypothesis for this work is Notum expression is affected by mechanical loading and aging. The goal of these studies is to investigate factors that could affect Notum expression, with the future direction of identifying factors that when pharmacologically modulated could promote anabolic bone growth. After establishing No-tum expression in the osteocyte cell line, MLOY4s, Notum expression was monitored in response to mechanical loading, mimicked via orbital shear stress for 15 min, 1hr, and 2hr. In addition, Notum expression was analyzed in aged bone. Our preliminary results suggest mechanical loading decreases Notum protein expression, while aging increases the expression of the Notum gene (p<0.05). . With these results our hypothesis is supported, and future studies repressing Notum expression in bone as novel approach to promoting anabolic bone growth will be conducted.
- Declaração de direitos:
- http://rightsstatements.org/vocab/InC/1.0/
- La langue:
- English
- Type:
- poster
- date créée:
- 11/22/2019
219. Role of peroxisome proliferator-activated receptor gamma (PPAR-γ) in Coxiella burnetii infection
- Title Tesim:
- Role of peroxisome proliferator-activated receptor gamma (PPAR-γ) in Coxiella burnetii infection
- Créateur:
- Mulye, Minal, Calhoun, Adelaide, and Spencer, Celina
- La description:
- Peroxisome proliferator-activated receptors (PPARs) are important nuclear receptors in regulating macrophage lipid metabolism and modulating cellular inflammatory responses. In recent years, host cell PPARs have been linked to bacterial pathogenesis and macrophage infections. Specifically, bacteria-induced manipulation of lipid droplets (LD), host lipid storage organelles, are directly associated with PPAR-γ activation. For example, the intracellular pathogens Mycobacterium bovis and M. leprae breakdown the macrophage LDs to release free fatty acids. These free fatty acids subsequently activate PPAR-γ to induce an anti-inflammatory immune response, thus sustaining Mycobacterial intracellular growth. Our previously published studies report that the intracellular bacterium Coxiella burnetii induces host cell LD breakdown to support its growth in macrophages. Coxiella is known to cause non-culturable endocarditis that can present up to 20 years post initial infection, suggesting its ability to survive long-term in the host by subverting the host immune response. Our overall goal is to identify the strategies that Coxiella employs to manipulate the host immune response. This could ultimately aid in developing therapeutic targets to inhibit Coxiella’s intracellular growth. Since LD breakdown is important for intracellular Coxiella growth through the release of free fatty acids (PPAR-γ agonists), we hypothesize that Coxiella infection activates host cell PPAR-γ to induce an anti-inflammatory environment which supports bacterial growth and infection. To test this hypothesis, we quantified PPAR-γ gene expression in Coxiella-infected macrophages using quantitative Real Time PCR (qRT-PCR) at different times post-infection. Compared to uninfected cells, infected macro-phages demonstrated increased PPAR-γ gene expression suggesting that Coxiella induces PPAR-γ activation. Ongoing studies are focused on identifying PPAR-γ tran-scriptional activity in Coxiella-infected cells and the downstream targets. Future studies will determine if PPAR-γ activity is dependent on host cell LD metabolism and identify potential PPAR-γ antagonists as therapeutic targets to inhibit Coxiella intracellular growth.
- Declaração de direitos:
- http://rightsstatements.org/vocab/InC/1.0/
- La langue:
- English
- Type:
- poster
- date créée:
- 11/22/2019
220. Role of peroxisome proliferator-activated receptor y (PPARy) in Coxiella burnetii infection
- Title Tesim:
- Role of peroxisome proliferator-activated receptor y (PPARy) in Coxiella burnetii infection
- Créateur:
- Mulye, Minal, Calhoun, Adelaide, and Spencer, Celina
- Related Url Tesim:
- Audio Presentation: https://marian.hosted.panopto.com/Panopto/Pages/Viewer.aspx?id=46fc6dd2-bf76-47c2-abe3-ac730000c7f4
- Declaração de direitos:
- http://rightsstatements.org/vocab/InC/1.0/
- La langue:
- English
- Type:
- Poster
- Mot-clé:
- peroxisome proliferator-activated receptor y (PPARy) and Coxiella burnetii
- date créée:
- 2020