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Title: 2014-2015 Program Review Dept of Biomedical Science.
Creator: Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
Date Issued: 2014-2015
PURL: http://purl.flvc.org/fau/fd/FA00007953
Subject Headings: Florida Atlantic University -- History
Format: Document (PDF)

Title: 2016-2017 Program Review Dept of Biomedical Science.
Creator: Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
Date Issued: 2016-2017
PURL: http://purl.flvc.org/fau/fd/FA00007955
Subject Headings: Florida Atlantic University -- History
Format: Document (PDF)

Title: 2015-2016 Program Review Dept of Biomedical Science.
Creator: Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
Date Issued: 2015-2016
PURL: http://purl.flvc.org/fau/fd/FA00007954
Subject Headings: Florida Atlantic University -- History
Format: Document (PDF)

Title: 2013-2014 Program Review Dept of Biomedical Science.
Creator: Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
Date Issued: 2013-2014
PURL: http://purl.flvc.org/fau/fd/FA00007952
Subject Headings: Florida Atlantic University -- History
Format: Document (PDF)

Title: tRNA processing and quality control in bacteria.
Creator: Alluri, Ravi Kumar, Li, Zhongwei, Charles E. Schmidt College of Science, Department of Biomedical Science
Abstract/Description: In this work, we report that the only exoribonuclease in M. genitalium, RNase R, is able to generate mature 3'-ends. The aminoacyl-acceptor stem, CCA terminus and discriminator residue plays an important role in stopping RNase R digestion at the mature 3'-end. Disruption of the stem causes partial or complete degradation of the pre-tRNA, whereas extension of the stem results in the formation of a mature 3’-end. CC residues in CCA terminus and A or G residues at discriminator position are the...
Show moreIn this work, we report that the only exoribonuclease in M. genitalium, RNase R, is able to generate mature 3'-ends. The aminoacyl-acceptor stem, CCA terminus and discriminator residue plays an important role in stopping RNase R digestion at the mature 3'-end. Disruption of the stem causes partial or complete degradation of the pre-tRNA, whereas extension of the stem results in the formation of a mature 3’-end. CC residues in CCA terminus and A or G residues at discriminator position are the most preferred residues for precise stopping of RNase R at mature 3’ end. The significance of this works shows that M. genitalium RNase R generates mature tRNA in a single step by recognizing features in the terminal domains of tRNA, a process requiring multiple RNases in most bacteria.
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Date Issued: 2013
PURL: http://purl.flvc.org/fau/fd/FA00004174
Format: Document (PDF)

Title: Peroxiredoxin 3 and Methionine sulfoxide reductase A are Essential for Lens Cell Viability by Preserving Lens Cell Mitochondrial Function through Repair of Cytochrome c.
Creator: Lee, Wanda, Florida Atlantic University, Kantorow, Marc, Charles E. Schmidt College of Science, Department of Biomedical Science
Abstract/Description: The central premise of this dissertation is that mitochondrial antioxidant enzymes are essential to lens cell viability by preserving lens cell mitochondria and protecting and/or repairing lens cell proteins, and two mitochondrial-specific antioxidant enzymes, Peroxiredoxin 3 (PRDX3) and Methionine sulfoxide reductase A (MsrA), are explored. In this dissertation, we will examine the expression ofPRDX3 in the human lens, its colocalization to the lens cell mitochondria, its ability to be...
Show moreThe central premise of this dissertation is that mitochondrial antioxidant enzymes are essential to lens cell viability by preserving lens cell mitochondria and protecting and/or repairing lens cell proteins, and two mitochondrial-specific antioxidant enzymes, Peroxiredoxin 3 (PRDX3) and Methionine sulfoxide reductase A (MsrA), are explored. In this dissertation, we will examine the expression ofPRDX3 in the human lens, its colocalization to the lens cell mitochondria, its ability to be induced by H20 2-oxidative stress, and speculate how PRDX3 function/sf could affect the lens. We will also examine the reduced levels of MsrA by targeted gene silencing and its effect on reactive oxygen species production and mitochondrial membrane potential in human lens cells to determine its role in mitochondrial function in the lens. Lastly, we will examine the ability of MsrA to repair and restore function to a critical mitochondrial protein, Cytochrome c. The collective evidence strongly indicates that the loss of mitochondrial-specific enzymes, such as PRDX3 and MsrA, are responsible for increased reactive oxygen species levels, decreased mitochondrial membrane potential, protein aggregation and lens cell death, and further indicates that mitochondrial repair, protective, and reducing systems play key roles in the progression of age-related cataract and other agerelated diseases.
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Date Issued: 2008
PURL: http://purl.flvc.org/fau/fd/FA00000868
Subject Headings: Genetic regulation, Proteins--Chemical modification, Cellular signal transduction, Eye--Physiology, Mitochondrial pathology
Format: Document (PDF)

Title: Reflections on the evolution of the vertebrate tissue inhibitors of metalloproteinases.
Creator: Brew, Keith
Date Issued: 2019-01-20
PURL: http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1096_fj.201801262R_1638460567
Format: Document (PDF)

Title: Inflammatory response in stress and the role of autophagy in breast cancer.
Creator: Onwuha-Ekpete, Lillian C., Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: We attempted to understand the molecular regulators that impact inflammation using a rat model of human sensation-seeking/risk-taking trait for drug and stress vulnerability, based on their exploratory behavior displaying high rates (HRs) or low rates of locomotor reactivity (LRs) to environmental stress. We found that HRs have a pro-inflammatory phenotype as indicated by increased protein expression of the inflammatory cytokine TNF-(Sa(B. Furthermore, we found that HRs have a lower gene...
Show moreWe attempted to understand the molecular regulators that impact inflammation using a rat model of human sensation-seeking/risk-taking trait for drug and stress vulnerability, based on their exploratory behavior displaying high rates (HRs) or low rates of locomotor reactivity (LRs) to environmental stress. We found that HRs have a pro-inflammatory phenotype as indicated by increased protein expression of the inflammatory cytokine TNF-(Sa(B. Furthermore, we found that HRs have a lower gene expression of the glucocorticoid receptor and histone deacetylase 2 which are known to play an immunosuppressive role. Autophagy (macroautophagy) is a homeostatic process needed for cell maintenance, growth and proliferation and known to assist in tumor survival. FYVE and coiled-coil domain containing 1 (FYCO1) is a novel protein implicated to assist in the plus-end directed trafficking and fusion of autophagosomes. In these studies, we show that FYCO1 gene expression among human breast cell lines of varying degrees of malignancy.
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Date Issued: 2012
PURL: http://purl.flvc.org/fcla/dt/3362042
Subject Headings: Breast, Cancer, Genetic aspects, Cancer, Molecular aspects, Carcinogenesis, Cellular signal transduction, Stress (Physiology)
Format: Document (PDF)

Title: An investigation of the role of PAK6 tumorigenesis.
Creator: Roberts, JoAnn, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: The function and role of PAK6, serine/threonone kinase, in cancer progressionhas not yet been clearly identified. Several studies reveal that PAK6 may participate in key changes contributing to cancer progression such as cell survival, cell motility, and invasiveness. Basedon the membrane localization of PAK6 in prostate and breast cancer cells,we speculated that PAK6 plays a rolein cancer progression cells by localizing on the membrane and modifying proteins linked to motility and...
Show moreThe function and role of PAK6, serine/threonone kinase, in cancer progressionhas not yet been clearly identified. Several studies reveal that PAK6 may participate in key changes contributing to cancer progression such as cell survival, cell motility, and invasiveness. Basedon the membrane localization of PAK6 in prostate and breast cancer cells,we speculated that PAK6 plays a rolein cancer progression cells by localizing on the membrane and modifying proteins linked to motility and proliferation. We isolated the raft domain of breast cancer cells expressing either wild type (WT), constitutively active (SN), or kinase dead PAK6 (KM) and found that PAK6 is a membrane associated kinase which translocates from the plasma membrane to the cytosol when activated. The downstream effects of PAK6 are unknown ; however, results from cell proliferation assays suggest a growth regulatory mechanism.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3356888
Subject Headings: Apoptosis, Cancer, Etiology, Cancer cells, Proliferation, Cellular signal transduction, Cellular control mechanisms, Cell cycle, Regulation
Format: Document (PDF)

Title: UP-regulation of inflammatory cytokines in the lacrimal glands of a predisposed mouse model of Sjèogren's syndrome (SS): the influence of sex hormones and a newly proposed mechanism for SS.
Creator: Czerwinski, Stefanie P.C., Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Sjèogren's Syndrome (SS) is a chronic, inflammatory autoimmune disease affecting mostly the exocrine cells of lacrimal and salivary glands, leading to diminished secretory function and resulting in keratoconjunctivitis sicca (dry eye disease) and/or stomatitis sicca (dry mouth disease). Despite several decades of studies focusing on autoimmune diseases and dry eye diseases, the exact etiology and mechanisms of SS remain unknown. Besides the fact that SS is often unreported, unrecognized and...
Show moreSjèogren's Syndrome (SS) is a chronic, inflammatory autoimmune disease affecting mostly the exocrine cells of lacrimal and salivary glands, leading to diminished secretory function and resulting in keratoconjunctivitis sicca (dry eye disease) and/or stomatitis sicca (dry mouth disease). Despite several decades of studies focusing on autoimmune diseases and dry eye diseases, the exact etiology and mechanisms of SS remain unknown. Besides the fact that SS is often unreported, unrecognized and untreated, today's therapies rely exclusively on treating the symptoms after disease progression; there exists neither prevention therapy nor cure for SS. In addition, SS has been diagnosed predominantly in post-menopausal women with the female to male ratio reaching 9:1, suggesting a role of ovarian sex hormones in the pathogenesis of SS. However, not all postmenopausal women develop SS, indicating the contribution of other factors such as a genetic background to the onset of SS. In the present study, ovariectomized (OVX) NOD.B10.H2b mice provide a model of menopause with a genetic predisposition to SS, as compared to non-predisposed C57BL/10 mice. Both strands of mice were either sham operated, OVX, OVX and treated with 17(Sb (Bestradiol (E2), or OVX and treated with dihydrotestosterone (DHT). Lacrimal glands were collected 3, 7, 21, and 30 days after surgery and processed for RNA analysis by rt-qPCR and protein assays by ELISA to evaluate cytokine expression and concentrations of IL- 1\U+fffd\, TNF-a, IFN-(Sd(B, IL-10, and IL-4 on a timeline. Overall, our results showed a significant increase in IL-1\U+fffd\ TNF-a, IL-10, and IL-4 expression and levels in the lacrimal glands of OVX NOD.B10.H2b mice as compared to sham operated animals, and treatment with E2 or DHT at time of OVX prevented the increase in cytokine expression and levels.
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Date Issued: 2013
PURL: http://purl.flvc.org/FAU/3360770
Subject Headings: Cytokines, Mice as laboratory animals, Dry eye syndromes, Immunological aspects, Sjèogren's syndrome, Immunological aspects, Medical genetics, Molecular immunology
Format: Document (PDF)

Title: Evaluation of cardiac function in cTnI(R192H) transgenic mice and cTni knockout mice with High-Resolution Ultrasound Imaging and Doppler Echocardiography.
Creator: Liu, Jing, Huang, Xupei, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Troponin I is a contractile protein and plays an important role in cardiac function. We have generated cTnl knockout and cTnI(R192H) transgenic mouse models. All of cTnl knockout homozygous mice die at 17-18 days after birth. Some of cTnI(R192H) transgenic mice die at early life stages, some mice develop heart failure at late stages. High-resolution ultrasound imaging and Doppler echocardiography have been used to evaluate cardiac function on cTnl deficient mice and cTnl(R192H) transgenic...
Show moreTroponin I is a contractile protein and plays an important role in cardiac function. We have generated cTnl knockout and cTnI(R192H) transgenic mouse models. All of cTnl knockout homozygous mice die at 17-18 days after birth. Some of cTnI(R192H) transgenic mice die at early life stages, some mice develop heart failure at late stages. High-resolution ultrasound imaging and Doppler echocardiography have been used to evaluate cardiac function on cTnl deficient mice and cTnl(R192H) transgenic mice. cTnI mice have damaged relaxation with gradually decreased E/A ratio(E/A<1). FS and cardiac output dramatically decrease on 17-day-o1d cTnI mice indicating severe cardiac dysfunction. We find that the damaged heart function is correspondent with the Tnl expression level decline. 6-8 weeks transgenic mice have shown that the dimension of left and right atria increase. In 15-month-old transgenic mice, the E/A ratio shows a pseudonormal pattern indicating a diastolic dysfunction. This study demonstrate that damaged heart function is tightly associated with Tnl levels in the heart.
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Date Issued: 2006
PURL: http://purl.flvc.org/fau/fd/FA00000789
Subject Headings: Transgenic mice, Mice as laboratory animals, Coronary heart disease--Seriodiagnosis, Congestive heart failure--Pathophysiology
Format: Document (PDF)

Title: Energy metabolism and slow skeletal troponin I phosphorylation in cardiac troponin I null mouse heart.
Creator: Jia, Yuanyuan, Florida Atlantic University, Huang, Xupei, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Troponin I (TnI) plays an important role in cardiac muscle contraction. Two TnI genes (cardiac and slow skeletal TnI) are predominantly expressed in the heart. In cTnI knockout mice, myocardial TnI deficiency results in a diastolic dysfunction and a sudden death in homozygous mutants. In the present studies, energy metabolism has been analyzed in myocardial cells from cTnI null hearts. Our results have demonstrated that damaged relaxation and increased Ca2+-independent force production in...
Show moreTroponin I (TnI) plays an important role in cardiac muscle contraction. Two TnI genes (cardiac and slow skeletal TnI) are predominantly expressed in the heart. In cTnI knockout mice, myocardial TnI deficiency results in a diastolic dysfunction and a sudden death in homozygous mutants. In the present studies, energy metabolism has been analyzed in myocardial cells from cTnI null hearts. Our results have demonstrated that damaged relaxation and increased Ca2+-independent force production in cTnI null hearts stimulated myofibril MgATPase activities accompanied by the increase of mitochondria quantity and ATPase activities. In addition, an increase of ssTnI phosphorylation level has been observed in cTnI null hearts. The results indicate that TnI deficiency can cause the disturbance of energy metabolism and some protein overphosphorylation.
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Date Issued: 2003
PURL: http://purl.flvc.org/fcla/dt/12998
Subject Headings: Mice as laboratory animals, Mice--Metabolism, Energy metabolism, Mitochondria
Format: Document (PDF)

Title: Mechanism and treatment of restrictive cardiomyopathy.
Creator: Jean-Charles, Pierre-Yves, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Restrictive cardiomyopathy (RCM) is a cardiac muscle disorder characterized by increased ventricular stiffness and diastolic dysfunction. Patients with RCM often present severe cardiac problems which usually lead to heart failure and sudden death. No effective treatment is available for RCM which makes the finding of novel efficient therapies an urgent necessity. Great progress in molecular biology techniques and advances in transgenic animal development provide great opportunities for the...
Show moreRestrictive cardiomyopathy (RCM) is a cardiac muscle disorder characterized by increased ventricular stiffness and diastolic dysfunction. Patients with RCM often present severe cardiac problems which usually lead to heart failure and sudden death. No effective treatment is available for RCM which makes the finding of novel efficient therapies an urgent necessity. Great progress in molecular biology techniques and advances in transgenic animal development provide great opportunities for the study of RCM and other cardiovascular diseases encountered in clinical patients.... Our laboratory is among the first to generate transgenic mouse models of RCM based on cardiac troponin I (cTnI) missense mutations. In this study, transgenic mice that suffer from RCM have been generated to understand the factors behind the diastolic dysfunction associated with that myocardial disease.... The information obtained from this study allows a better understanding of the role of troponin in RCM and the factors behind the physiopathology of the disease. It will also offer a therapeutic strategy taking into account the physiological characteristic of RCM.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3358554
Subject Headings: Biochemical markers -- Diagnostic use, Cardiovascular system -- Pathophysiology, Coronary heart disease -- Molecular diagnosis, Mice as laboratory animals, Molecular biology
Format: Document (PDF)

Title: Study on the Role oftmRNA in Protecting Escherichia coli Cell Under Oxidative stress.
Creator: Kollipara, Gayatri, Li, Zhongwei, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: tmRNA is a small stable RNA present in Eubacteria. Through a mechanism called trans-translation, tmRNA mediates ribosome rescue and quality control of proteins and mRNA. In this study, the Escherichia coli (E. coli) mutant lacking tmRNA was demonstrated hypersensitive to oxidative stress. The role of tmRNA-mediated surveillance mechanism in protecting E. coli cell under oxidative stress condition was examined. The tmRNA-mediated tagged protein levels were elevated in cells under oxidative...
Show moretmRNA is a small stable RNA present in Eubacteria. Through a mechanism called trans-translation, tmRNA mediates ribosome rescue and quality control of proteins and mRNA. In this study, the Escherichia coli (E. coli) mutant lacking tmRNA was demonstrated hypersensitive to oxidative stress. The role of tmRNA-mediated surveillance mechanism in protecting E. coli cell under oxidative stress condition was examined. The tmRNA-mediated tagged protein levels were elevated in cells under oxidative stress condition, demonstrating the enhanced need for tmRNA under such condition. Our results suggest that mRNA damage by oxidative stress may cause reduced cell viability, and that tmRNA is required to rescue cells under such condition. Furthermore, our observations showed that tmRNA is required for the optimal growth of E. coli under normal aeration but not under anaerobic condition, suggesting that oxidation ofmRNA is the major reason for requirement oftmRNA during normal aeration.
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Date Issued: 2007
PURL: http://purl.flvc.org/fau/fd/FA00000782
Subject Headings: Proteins--Synthesis, Bacterial genetics, Escherichia coli infections, Cells--Evolution
Format: Document (PDF)

Title: CELLULAR REQUIREMENTS FOR MBLAC1 EXPRESSION AS ASSESSED IN MBLAC1-/- MOUSE EMBRYONIC FIBROBLASTS.
Creator: McGovern, Samantha, Blakely, Randy, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Science
Abstract/Description: The majority of research on drug addiction centers on dopamine (DA)- driven synaptic plasticities and how these changes ultimately lead to compulsive drug seeking. However, growing evidence supports a role of glial factors in various steps that lead to drug abuse and addiction. In this regard, significant evidence implicates glial glutamate (Glu) transporters (GLT-1) and cystine/Glu exchangers (xCT) in determining synaptic and extrasynaptic levels of Glu that support the acute and chronic...
Show moreThe majority of research on drug addiction centers on dopamine (DA)- driven synaptic plasticities and how these changes ultimately lead to compulsive drug seeking. However, growing evidence supports a role of glial factors in various steps that lead to drug abuse and addiction. In this regard, significant evidence implicates glial glutamate (Glu) transporters (GLT-1) and cystine/Glu exchangers (xCT) in determining synaptic and extrasynaptic levels of Glu that support the acute and chronic actions of drugs of abuse. -lactam antibiotics have been found in rodent models to upregulate CNS GLT-1 and xCT and thereby contribute to reinstatement after chronic drug exposure and withdrawal. Previously, the Blakely lab identified a glial expressing gene, swip-10, in Caenorhabditis elegans, whose deletion results in the hyperdominergic phenotype Swimming-Induced Paralysis (Swip), supported by Glu signalingdependent DA neuron hyperexcitability that ultimately drives oxidative stress and DA neuron degeneration. Both SWIP-10 and its putative mammalian ortholog MBLAC1 possess a highly conserved metallo -lactamase domain, and MBLAC1 has been found to bind the Glu modulating, b-lactam antibiotic ceftriaxone (Cef). Indeed, immunodepletion studies indicate that MBLAC1 may be the major highaffinity Cef-binding protein in the brain, leading to the hypothesis that MBLAC1 has a Glu modulatory role(s). Recently a functional role of MBLAC1 been proposed, involving activity as a 3’ exonuclease that processes polyA- mRNAs, including RNAs encoding cell replication-dependent histones. How this role, or others, may support the actions of MBLAC1 in the brain and the non-microbial actions of Cef to extracellular Glu homeostasis, is unclear. Recently, the Blakely lab generated Mblac1-/- mice as a tool to investigate these issues. The following work investigated the requirements of MBLAC1 in growth and the actions of Cef in mouse embryonic fibroblasts (MEFs) cultured from either Mblac1+/+ and Mblac1-/- mice. The presented data suggested that Mblac1-/- MEFs display attenuated growth and cell proliferation relative to Mblac1+/+ MEFs. For the first time, the in vitro protective actions of Cef against oxidative stress is shown to be dependent on MBLAC1. The following studies presented contribute to a definition of the role of MBLAC1 and as a Cef binding protein in native preparations, with findings that can drive models for the role of MBLAC1 in the CNS.
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Date Issued: 2019
PURL: http://purl.flvc.org/fau/fd/FA00013395
Subject Headings: Drug addiction--Research, Amino Acid Transport System X-AG, Mice, Fibroblasts
Format: Document (PDF)

Title: Developmental and Protective Mechanisms of the Ocular Lens.
Creator: Chauss, Daniel C., Kantorow, Marc, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biomedical Science
Abstract/Description: The vertebrate eye lens functions to focus light onto the retina to produce vision. The lens is composed of an anterior monolayer of cuboidal epithelial cells that overlie a core of organelle free fiber cells. The lens develops and grows throughout life by the successive layering of lens fiber cells via their differentiation from lens epithelial cells. Lens developmental defect and damage to the lens are associated with cataract formation, an opacity of the lens that is a leading cause of...
Show moreThe vertebrate eye lens functions to focus light onto the retina to produce vision. The lens is composed of an anterior monolayer of cuboidal epithelial cells that overlie a core of organelle free fiber cells. The lens develops and grows throughout life by the successive layering of lens fiber cells via their differentiation from lens epithelial cells. Lens developmental defect and damage to the lens are associated with cataract formation, an opacity of the lens that is a leading cause of visual impairment worldwide. The only treatment to date for cataract is by surgery. Elucidating those molecules and mechanisms that regulate the development and lifelong protection of the lens is critical toward the development of future therapies to prevent or treat cataract. To determine those molecules and mechanisms that may be important for these lens requirements we employed high-throughput RNA sequencing of microdissected differentiation statespecific lens cells to identify an extensive range of transcripts encoding proteins expressed by these functionally distinct cell types. Using this data, we identified differentiation state-specific molecules that regulate mitochondrial populations between lens epithelial cells that require the maintenance of a functional population of mitochondria and lens fiber cells that must eliminate their mitochondria for their maturation. In addition, we discovered a novel mechanism for how lens epithelial cells clear apoptotic cell debris that could arise from damage to the lens and found that UVlight likely compromises this system. Moreover, the data herein provide a framework to determine novel lens cell differentiation state-specific mechanisms. Future studies are required to determine the requirements of the identified molecules and mechanisms during lens development, lens defense against damage, and cataract formation.
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Date Issued: 2016
PURL: http://purl.flvc.org/fau/fd/FA00004577
Subject Headings: Eye--Diseases--Etiology., Cell differentiation., Cellular signal transduction., Protein folding., Mitochondrial pathology., Cellular control mechanisms., Apoptosis., Oxidative stress--Prevention.
Format: Document (PDF)

Title: EFFECTS OF SPECIFIC PfEMP1 LIGATION INTERACTIONS WITH ICAM-1, INTEGRIN αVβ3, AND CD36 ON MONOCYTES IN AN IN VITRO MALARIANAÏVE HOST MODEL.
Creator: Merritt, Jordan, Oleinikov, Andrew, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Science
Abstract/Description: Malaria is a severe global health problem that causes approximately 435,000 deaths per year. Any non-immune individual traveling to malaria endemic regions can be affected too, including humanitarian volunteers, travelers, and US troops. Under physiological conditions, damaged or malaria-infected RBCs would be removed within the spleen, but Plasmodium falciparum infected RBCs (iRBCs) sequester to microvascular endothelial cells to avoid entering the spleen. Adhesion interactions and parasite...
Show moreMalaria is a severe global health problem that causes approximately 435,000 deaths per year. Any non-immune individual traveling to malaria endemic regions can be affected too, including humanitarian volunteers, travelers, and US troops. Under physiological conditions, damaged or malaria-infected RBCs would be removed within the spleen, but Plasmodium falciparum infected RBCs (iRBCs) sequester to microvascular endothelial cells to avoid entering the spleen. Adhesion interactions and parasite sequestration to endothelial cells are mediated by Plasmodium falciparum erythrocyte membrane protein 1 family (PfEMP1) proteins expressed on the iRBC’s surface. The PfEMP1 proteins bind to existing endothelial cell surface receptors that already serve primary functions, including ICAM-1, integrin αVβ3, and CD36. Traditionally, these receptors are explored in the context of endothelial cell sequestration, but this project examines the consequence of receptor::PfEMP1 interaction on immune cells, namely monocyte-like THP-1 cells.
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Date Issued: 2019
PURL: http://purl.flvc.org/fau/fd/FA00013398
Subject Headings: Malaria, Plasmodium falciparum, Integrins, Monocytes, Intercellular Adhesion Molecule-1, CD36 Antigens, Adhesiveness
Format: Document (PDF)

Title: Elucidating the role of Semaphorin 7A in breast cancer.
Creator: Garcia-Areas, Ramon A., lragavarapu-Charyulu, Vijaya, Florida Atlantic University, Charles E Schmidt College of Science, Department of Biomedical Science
Abstract/Description: Solid tumors can hijack many of the same programs used in neurogenesis to enhance tumor growth and metastasis, thereby generating a plethora of neurogenesis-related molecules including semaphorins Among them, we have identified Semaphorin7A (SEMA7A) in breast cancer We first used to the DA-3 mammary tumor model to determine the effect of tumor-derived SEMA7A on immune cells We found that tumor-derived SEMA7A can modulate the production of proangiogenic chemokines CXCL2/MIP-2 and CXCL 1, and...
Show moreSolid tumors can hijack many of the same programs used in neurogenesis to enhance tumor growth and metastasis, thereby generating a plethora of neurogenesis-related molecules including semaphorins Among them, we have identified Semaphorin7A (SEMA7A) in breast cancer We first used to the DA-3 mammary tumor model to determine the effect of tumor-derived SEMA7A on immune cells We found that tumor-derived SEMA7A can modulate the production of proangiogenic chemokines CXCL2/MIP-2 and CXCL 1, and prometastatic MMP-9 in macrophages We next aimed to determine the expression and function of SEMA7A in mammary tumor cells We found that SEMA7A is highly expressed in both metastatic human and murine breast cancer cells We show that both TGF-β and hypoxia elicits the production of SEMA 7 A in mammary cells SEMA7 A shRNA silencing in 4T1 cells resulted in decreased mesenchymal markers MMP-3, MMP-13, Vimentin and TGF-β) SEMA7A silenced cells show increased stiffness with reduced migratory and proliferative potential In vivo, SEMA7A silenced 4T1 tumor bearing mice showed decreased tumor growth and metastasis Genetic ablation of host-derived SEMA7A synergized to further decrease the growth and metastasis of 4T1 cells Our findings suggest novel functional roles for SEMA7A in breast cancer and that SEMA7A could be a novel therapeutic target to limit tumor growth and metastasis
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Date Issued: 2016
PURL: http://purl.flvc.org/fau/fd/FA00004802
Subject Headings: Breast--Cancer--Diagnosis, Semaphorins, Protein precursors, Cellular signal transduction, Cell receptors
Format: Document (PDF)

Title: Unraveling the molecular mechanism of human polynucleotide phosphorylase (hPNPase) in controlling oxidized RNA.
Creator: Malla, Sulochan, Li, Zhongwei, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Science
Abstract/Description: Oxidation by reactive oxygen species is the major source of RNA damaging insult in living organisms. Increased RNA oxidation has been strongly implicated in a wide range of human diseases; predominantly neurodegeneration. Oxidized RNA should be removed from the cellular system to prevent their deleterious effect to the cells and organisms. In eukaryotic cells, mitochondria are the major intracellular sources of ROS and may cause greater damage to the mitochondrial RNA. In this study, we first...
Show moreOxidation by reactive oxygen species is the major source of RNA damaging insult in living organisms. Increased RNA oxidation has been strongly implicated in a wide range of human diseases; predominantly neurodegeneration. Oxidized RNA should be removed from the cellular system to prevent their deleterious effect to the cells and organisms. In eukaryotic cells, mitochondria are the major intracellular sources of ROS and may cause greater damage to the mitochondrial RNA. In this study, we first investigated the RNA oxidation, by measuring the level of 8-hydroxy-Guanosine (8-oxo-Guo), inside mitochondria and cytoplasm in cultured human cells. We discovered that the mitochondrial 8-oxo-Guo is higher than its cytoplasmic counterparts under both normal growth and oxidative stress condition. Next, we explored the role of human polynucleotide phosphorylase (hPNPase) in controlling RNA oxidation inside mitochondria and cytoplasm. hPNPase binds to oxidized RNA with higher affinity, reduces the 8-oxo-Guo level in total RNA and protects cells against oxidative stress. In this study, the molecular mechanism of hPNPase in 8-oxo-Guo reduction was investigated. First, the effect of hPNPase activities on the 8-oxo-Guo level in mitochondria and cytoplasm was examined. The knockdown of hPNPase increased both the mitochondrial and cytoplasmic 8-oxo-Guo, whereas overexpression had the opposite effect. Second, our study revealed that hSUV3, an RNA helicase that forms a functional complex with hPNPase in mitochondria, was dispensable in reducing 8-oxo-Guo levels.
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Date Issued: 2019
PURL: http://purl.flvc.org/fau/fd/FA00013392
Subject Headings: RNA, Reactive Oxygen Species, Mitochondria, Oxidative stress
Format: Document (PDF)

Title: Protective Mechanisms of Granulocyte-Colony Stimulating Factor Against Experimental Models of Stroke.
Creator: Menzie-Suderam, Janet, Wu, Jang-Yen, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biomedical Science
Abstract/Description: Ischemic stroke has a multiplicity of pathophysiological mechanisms. Granulocyte-colony stimulating factor (G-CSF) is an endogenous growth factor that exerts a diverse range of neuroprotection against ischemic stroke. Several lines of evidence demonstrated the contribution of endoplasmic reticulum (ER) in apoptotic cell death involving ischemia. Cell culture of undifferentiated PC12 cells were subjected to 10mM glutamate and selected doses of G-CSF (25ng/ml, 50ng/ml, 100ng/ml and 250ng/ml)...
Show moreIschemic stroke has a multiplicity of pathophysiological mechanisms. Granulocyte-colony stimulating factor (G-CSF) is an endogenous growth factor that exerts a diverse range of neuroprotection against ischemic stroke. Several lines of evidence demonstrated the contribution of endoplasmic reticulum (ER) in apoptotic cell death involving ischemia. Cell culture of undifferentiated PC12 cells were subjected to 10mM glutamate and selected doses of G-CSF (25ng/ml, 50ng/ml, 100ng/ml and 250ng/ml) for 24 hours. Cell viability, expression of the G-CSF receptor and expression level of CHOP were assessed in vitro. Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO). Rats were subcutaneously injected with G-CSF (n= 15; 50ug/kg body weight) 24 hours post-MCAO for 4 days. Vehicle treated rats were administered 5% dextrose for 1 day (n=4) or 4 days (n=16). Sham-operated rats (n=9) were not subjected to MCAO. Neurological deficit and infarct volume were measured while expression levels of pAKT, Bcl2, Bax, Bak, cleaved caspase-3, GRP78, ATF4, ATF6, p-p38MAPK, pJNK, CHOP and HSP27 were analyzed by western blotting. In vitro G-CSF receptor was expressed on undifferentiated PC12 cell, and an optimal dose of 50 ng/ml G-CSF significantly protected these cells against glutamate-induced cytotoxicity (P < 0.05). G-CSF significantly down-regulated (P < 0.01) the ER stressinduced pro-apoptotic marker CHOP in vitro. In vivo, G-CSF reduced infarct volume to 50% while significantly improved neurological deficit compared to vehicle rats. G-CSF significantly (P < 0.05) up-regulated pro-survival proteins pAKT and Bcl2 while downregulating pro-apoptotic proteins Bax, Bak and cleaved caspase 3 in the ischemic brain. It also significantly (P < 0.05) downregulated the ER intraluminal stress sensor GRP78, proteins of ER stress induced intracellular pathway; ATF4, ATF6, p-p38MAPK, pJNK and the ER stress induced apoptotic marker CHOP, which suggests that ER stress is being ameliorated by G-CSF treatment. G-CSF also reduced the level of HSP27, providing additional evidence of cellular stress reduction. G-CSF treatment increased cell survival by attenuating both general pro-apoptotic proteins and specific effector proteins in the ER stress induced apoptotic pathways. Our data has provided new insight into the anti-apoptotic mechanism of G-CSF, especially as it relates to ER stress induced apoptosis in ischemia.
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Date Issued: 2016
PURL: http://purl.flvc.org/fau/fd/FA00004795, http://purl.flvc.org/fau/fd/FA00004795
Subject Headings: Cerebral ischemia--Protection., Apoptosis., Rats as laboratory animals., Cellular signal transduction., Oxidation-reduction reaction.
Format: Document (PDF)

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