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Title: Effects of Sulindac and Taurine on Glutamate Induced Exocitoxicity and Hypoxia Induced Cell Death.
Creator: D'Errico, Anthony, Pan, Chunliu, Prentice, Howard
Abstract/Description: FAU's Office of Undergraduate Research and Inquiry hosts an annual symposium where students engaged in undergraduate research may present their findings either through a poster presentation or an oral presentation.
Date Issued: 2011
PURL: http://purl.flvc.org/fau/fd/FA00005431
Format: Document (PDF)

Title: Mechanism of taurine protection against endoplasmic reticulum stress induced by glutamate in primary cortical neurons.
Creator: Pan, Chunliu, Wu, Jang-Yen, Prentice, Howard, Graduate College
Date Issued: 2011-04-08
PURL: http://purl.flvc.org/fcla/dt/3164675
Subject Headings: Taurine, Endoplasmic reticulum, Glutamates
Format: Document (PDF)

Title: The NSAID, Sulindac confers protection against oxidative stress induced damage in retinal pigmented epithelial cells.
Creator: Sur, Arunodoy, Biswal, Manas, Kreymerman, Alexander, Weissbach, Herbert, Prentice, Howard, Blanks, Janet C., Graduate College
Date Issued: 2011-04-08
PURL: http://purl.flvc.org/fcla/dt/3164798
Subject Headings: Nonsteroidal anti-inflammatory agents, Oxidative stress, Epithelial cells
Format: Document (PDF)

Title: Role of taurine in the central nervous system.
Creator: Wu, Jang-Yen, Prentice, Howard
Date Issued: 2010-08-24
PURL: http://purl.flvc.org/fau/fd/FADT3327262
Subject Headings: Central Nervous System --metabolism, Glutamic Acid --metabolism, Homeostasis --physiology, Neuroprotective Agents --metabolism, Neurotransmitter Agents --metabolism, Proto-Oncogene Proteins c-bcl-2 --metabolism, Receptors, Neurotransmitter --metabolism, Signal Transduction --physiology, Taurine, Taurine --metabolism, Neuroprotective Agents, Neurotransmitter Agents
Format: Document (PDF)

Title: Protection of taurine and granulocyte colony-stimulating factor against excitotoxicity induced by glutamate in primary cortical neurons.
Creator: Pan, Chunliu, Gupta, Amit, Prentice, Howard, Wu, Jang-Yen
Date Issued: 2010-08-24
PURL: http://purl.flvc.org/fcla/dt/3329093
Format: Document (PDF)

Title: Materials and Methods for the Treatment of Pathological Neovascularization in the Eye, 2012.
Creator: Blanks, Janet C., Prentice, Howard M., Florida Atlantic University, Dorey, C. Kathleen
Abstract/Description: The subject invention provides materials and methods useful in safely and effectively preventing pathological proliferation of blood vessels. The prevention of the over-proliferation of blood vessels according to the subject invention is particularly advantageous for treatment of certain ocular conditions including age-related macular degeneration (AMD), retinopathy of prematurity (ROP) and diabetic retinopathy. In preferred embodiments, the subject invention provides materials and methods...
Show moreThe subject invention provides materials and methods useful in safely and effectively preventing pathological proliferation of blood vessels. The prevention of the over-proliferation of blood vessels according to the subject invention is particularly advantageous for treatment of certain ocular conditions including age-related macular degeneration (AMD), retinopathy of prematurity (ROP) and diabetic retinopathy. In preferred embodiments, the subject invention provides materials and methods for effective treatment of pathological ocular neovascularization using gene therapy. In a specific embodiment the materials and methods of the subject invention can be used to treat AMD.
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Date Issued: 2012
PURL: http://purl.flvc.org/fau/fd/FAUIR000245
Format: Document (PDF)

Title: GFAP-Based Gene Therapy for Treatment of Retinal Diseases, 2008.
Creator: Dorey, C. Kathleen, Blanks, Janet C., Florida Atlantic University, Prentice, Howard
Abstract/Description: Compositions and methods for reducing neovascularization. Purified nucleic acid constructs and vectors encoding an antiangiogenic protein operably linked to a GFAP promoter. Vectors can include at least one hypoxia regulated element, enhancer element and silencer element. Gene therapy methods for reducing, delaying or preventing neovascularization based on the nucleic acid constructs and vectors.
Date Issued: 2008
PURL: http://purl.flvc.org/fau/fd/FAUIR000259
Format: Document (PDF)

Title: Tissue Protection and Cell Death Pathways in Myocardial Ischemia.
Creator: Rickaway, Zach T., Prentice, Howard, Florida Atlantic University
Abstract/Description: The excess generation of Reactive oxygen species (ROS) can damage cell components and disrupt cellular functions. Methionine in proteins is easily oxidized by ROS and converted to methionine sulfoxide. The enzyme peptide Methionine Sulfoxide Reductase reduces methionine sulfoxide back to methionine. We report here that MsrA over expression in rat cardiac myocytes prevents damage from ROS and increases cell viability after hypoxic/reoxygenation events. The nonsteroidal anti-inflamatory drug ...
Show moreThe excess generation of Reactive oxygen species (ROS) can damage cell components and disrupt cellular functions. Methionine in proteins is easily oxidized by ROS and converted to methionine sulfoxide. The enzyme peptide Methionine Sulfoxide Reductase reduces methionine sulfoxide back to methionine. We report here that MsrA over expression in rat cardiac myocytes prevents damage from ROS and increases cell viability after hypoxic/reoxygenation events. The nonsteroidal anti-inflamatory drug (NSAID) sulindac contains a methyl sulfoxide moiety that can scavenge ROS. Sulindac can be reduced by MsrA and contribute as an antioxidant in the cell. Our results demonstrate that 1 OOuM sulindac can reduce cell death in rat cardiac myocytes during hypoxia/reoxygenation, and ischemia/reperfusion in Langendorf[ perfusions. The BNIP proteins are pro-apoptotic members of the Bcl-2 family of apoptosis regulating proteins. Hypoxia/acidosis stabilizes BNIP-3 and increases its association with the mitochondria, causing the release of cytochrome C and cell death. We report the retrograde perfusion Langendorffmodel is inconclusive in mouse hearts.
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Date Issued: 2006
PURL: http://purl.flvc.org/fau/fd/FA00000820
Subject Headings: Mitochondrial pathology, Heart--Pathophysiology, Apoptosis, Cell differentiation
Format: Document (PDF)

Title: Calpain Cleavage of GAD65 is pathological and impairs gaba neurotransmission.
Creator: Buddhala, Chandana, Suarez, Marjorie, Alexandrescu, Anamaria, Pissaris, Adam, Modi, Jigar P., Wei, Jianning, Prentice, Howard, Wu, Jang-Yen, Graduate College
Date Issued: 2011-04-08
PURL: http://purl.flvc.org/fcla/dt/3164511
Subject Headings: Nervous System Diseases, GABA --physiology, Gamma-aminoboterzuur
Format: Document (PDF)

Title: GFAP-based gene therapy for treatment of retinal diseases.
Creator: Dorey, C. Kathleen, Blanks, Janet C., Prentice, Howard, Florida Atlantic University
Date Issued: 2005-11
PURL: http://purl.flvc.org/fcla/dt/15800
Format: Document (PDF)

Title: Taurine protection of PC12 cells against endoplasmic reticulum stress induced by oxidative stress.
Creator: Pan, Chunliu, Giraldo, Grace S., Prentice, Howard, Wu, Jang-Yen
Date Issued: 2010-08-24
PURL: http://purl.flvc.org/fcla/dt/3327276
Subject Headings: Oxidative Stress, Oxidative Stress --drug effects, Oxidative Stress --physiology, Antioxidants --pharmacology, Apoptosis Regulatory Proteins, Proto-Oncogene Proteins c-bcl-2, PC12 Cells --drug effects, Endoplasmic Reticulum --drug effects, Transcription Factor CHOP, Taurine
Format: Document (PDF)

Title: Taurine inhibits glutamate-induced excitotoxicity through a calpain dependent pathway.
Creator: Leon, Rebecca, Prentice, Howard, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Taurine, an endogenous ammo acid and neuromodulator, has been found to be neuroprotective against numerous forms of neurotoxicity including glutamate-induced excitotoxicity. Previously we have shown that taurine inhibits glutamate-induced calcium influx through VGCCs and NMDA receptors. Although the neuroprotective effects of taurine against excitotoxicity have been attributed to its intracellular Ca2+ regulatory functions, the complete mechanism underling taurine neuroprotection has remained...
Show moreTaurine, an endogenous ammo acid and neuromodulator, has been found to be neuroprotective against numerous forms of neurotoxicity including glutamate-induced excitotoxicity. Previously we have shown that taurine inhibits glutamate-induced calcium influx through VGCCs and NMDA receptors. Although the neuroprotective effects of taurine against excitotoxicity have been attributed to its intracellular Ca2+ regulatory functions, the complete mechanism underling taurine neuroprotection has remained unclear. Using primary rat cortical neuronal cell cultures, we have determined key cytosolic components to the mechanism of taurine neuroprotection. In this study we have found that taurine inhibits excitotoxicity by suppressing glutamate-induced elevations in [Ca2+]i, preventing calpain activation, and inhibiting reductions in Bel- 2:Bax ratios and consequently activation of the intrinsic pathway.
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Date Issued: 2008
PURL: http://purl.flvc.org/fau/fd/FA00000788
Subject Headings: Cellular signal transduction, Taurine--Physiological effect, Proteolytic enzymes--Research
Format: Document (PDF)

Title: Calpain Cleavage of Brain Glutamic Acid Decarboxylase 65 Is Pathological and Impairs GABA Neurotransmission.
Creator: Buddhala, Chandana, Suarez, Marjorie, Modi, Jigar P., Prentice, Howard, Ma, Zhiyuan, Tao, Rui, Wu, Jang-Yen, Smalheiser, Neil R.
Date Issued: 2012-03-12
PURL: http://purl.flvc.org/fau/fd/FAUIR000097
Format: Citation

Title: G-CSF GENE THERAPY FOR BRAIN DISEASES AND/OR SICKLE CELL ANEMIA.
Creator: Basilio, Stefan, Prentice, Howard, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
Abstract/Description: Ischemic stroke is defined as a blockage or reduced flow of blood to select areas of brain tissue due to either plaque formation or buildup of blood clots in the small blood vessels. A characteristic of sickle cell anemic patients is the potential for them to experience a similar type of blockage due to the sticky nature of the sickled red blood cells as well as defective oxygen delivery to the brain. Because of this similarity, sickle cell anemia may represent a good animal research model...
Show moreIschemic stroke is defined as a blockage or reduced flow of blood to select areas of brain tissue due to either plaque formation or buildup of blood clots in the small blood vessels. A characteristic of sickle cell anemic patients is the potential for them to experience a similar type of blockage due to the sticky nature of the sickled red blood cells as well as defective oxygen delivery to the brain. Because of this similarity, sickle cell anemia may represent a good animal research model for therapeutic intervention based on stroke models. In recent studies, Granulocyte-Colony Stimulating Factor (GCSF), has been shown to exhibit a robust range of neuroprotective properties against neurological disorders including ischemic stroke through preservation of the endoplasmic reticulum (ER) by modulating various ER stress pathways. Through cognitive deficit analysis in the form of behavioral and locomotor experiments in addition to in situ biomarker analysis by way of western blotting and immunohistochemistry, we found that G-CSF gene therapy exhibited neurogenic and neuroprotective effects in ischemic mouse models and could possibly serve as a good therapy for other diseases that share similar pathology to stroke.
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Date Issued: 2021
PURL: http://purl.flvc.org/fau/fd/FA00013787
Subject Headings: Sickle cell anemia, Stroke, Granulocyte Colony-Stimulating Factor, Gene therapy
Format: Document (PDF)

Title: A CELL BIOLOGICAL AND ELECTROPHYSIOLOGICAL STUDY OF MOUSE RETINA.
Creator: Sullivan, James P., Shen, Wen, Prentice, Howard, Florida Atlantic University, Center for Complex Systems and Brain Sciences, Charles E. Schmidt College of Science
Abstract/Description: Both proliferative diabetic retinopathy and exudative age-related macular degeneration are major causes of blindness which are caused by growth of defective, leaky and tortuous blood vessels in the retina. Hypoxia is implicated in triggering both of these diseases and results in induction of HIF-1alpha transcription factor in addition to the angiogenic factor VEGF. Müller cells are the major glial cell in the retina and they contribute to neovascularization in hypoxic regions of the retina...
Show moreBoth proliferative diabetic retinopathy and exudative age-related macular degeneration are major causes of blindness which are caused by growth of defective, leaky and tortuous blood vessels in the retina. Hypoxia is implicated in triggering both of these diseases and results in induction of HIF-1alpha transcription factor in addition to the angiogenic factor VEGF. Müller cells are the major glial cell in the retina and they contribute to neovascularization in hypoxic regions of the retina through eliciting secretion of growth factors, cytokines and angiogenic factors. As Müller cells span the breadth of the retina they can secrete angiostatic factors as well as neuroprotective trophic factors, the Müller cell is a valuable cell type for targeting by potential new gene therapies. The current investigation tests the hypoxia responsiveness of an AAV vector containing a hybrid hypoxia response element together with a GFAP promoter, and this vector encodes the angiostatic protein decorin, a well characterized multi-receptor tyrosine kinase inhibitor. Decorin may have advantages over other key angiostatic factors such as endostatin or angiostatin by virtue of its multiple anti-angiogenic signaling modalities. We employed Q-RT-PCR to evaluate the cell specificity and hypoxia responsiveness of an AAV-Vector termed AAV-REG-Decorin containing a hybrid HRE and GFAP promoter driving expression of the decorin transgene. The vector also contains a silencer element between the HRE and the GFAP domains to enable low basal expression in normoxia as well as high level inducibility in hypoxia. AAV-REGDecorin was found to elicit high level expression of decorin mRNA in hypoxia with greater than 9 – fold induction of the transgene in hypoxic conditions in astrocytes by comparison to normoxic astrocytes. AAV-REG-Decorin showed low levels of transgene expression by comparison to the positive control vector AAV-CMV -decorin containing the ubiquitously active CMV-promoter. The expression levels of decorin mRNA from AAV-REG-Decorin and from AAV-GFAP-Decorin were low in the PC12 neuronal cell model and in the ARPE19 line of retinal pigment epithelial cells with respect to those of AAV-CMV-decorin and no induction of Decorin mRNA was found with AAV-REGDecorin in these two control cell lines. Our novel gene therapy vector will serve as a platform for testing efficacy in rodent disease models (OIR and laser induced choroidal neovascularization) for assessment of the benefits of tightly regulated antiangiogenic gene therapy eliciting decorin transgene expression, both in terms of timing and the cellular source of production, during the progression of the retinal pathophysiology.
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Date Issued: 2021
PURL: http://purl.flvc.org/fau/fd/FA00013725
Subject Headings: Macular Degeneration, Retina, Gene therapy, Decorin
Format: Document (PDF)

Title: THERAPEUTIC STRATEGIES USING SULINDAC AND G-CSF GENE THERAPY FOR NEUROLOGICAL DISEASE.
Creator: Chen, Belinda, Prentice, Howard, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
Abstract/Description: Alzheimer’s disease is a neurodegenerative disease that causes cognitive dysfunction and leads to progressive memory loss and behavioral impairment. About 60% to 80% of dementia cases are attributed to Alzheimer’s disease and currently afflict about 50 million people worldwide. Although it primarily affects people over the age of 65, a person’s risk for developing Alzheimer’s disease earlier can depend on factors such as a family history (genetic inheritance) or experiencing an ischemic...
Show moreAlzheimer’s disease is a neurodegenerative disease that causes cognitive dysfunction and leads to progressive memory loss and behavioral impairment. About 60% to 80% of dementia cases are attributed to Alzheimer’s disease and currently afflict about 50 million people worldwide. Although it primarily affects people over the age of 65, a person’s risk for developing Alzheimer’s disease earlier can depend on factors such as a family history (genetic inheritance) or experiencing an ischemic stroke event. Current treatments for Alzheimer’s disease include behavioral therapy and drug treatment that can lessen the severity of symptoms but cannot stop progression indefinitely. Sulindac is a non-steroidal anti-inflammatory drug that, by a mechanism independent of its anti-inflammatory properties, has shown to express a preconditioning response to protect from oxidative damage. Granulocyte colony stimulating factor is a hematopoietic glycoprotein that can stimulate the production of granulocytes and stem cells that has proven to provide neuroprotection in models of ischemic stroke via mechanisms including anti-apoptosis and anti-inflammation. In this in vitro study, the potential neuroprotective effects of Sulindac is measured against the effects of oxidative stress when subjected to hypoxia and reperfusion. Regarding un-transfected SHSY-5Y cells, hypoxia was demonstrated to lower cell viability starting at a period of 12 hours. It was found that a low concentration of Sulindac (200 uM) was effective in protecting SHSY-5Y cells against oxidative stress and overall lowering the rate of cell death in the event of hypoxic and reperfusion injury. When SHSY-5Y cells were transfected with Swedish APP mutation, cell viability was also markedly decreased in hypoxic conditions. However when treated with a concentration of 600 uM of Sulindac, cell viability levels were near matched with its normoxic counterparts
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Date Issued: 2022
PURL: http://purl.flvc.org/fau/fd/FA00014021
Subject Headings: Sulindac, Granulocyte-colony stimulating factor, Genetic Therapy, Alzheimer Disease
Format: Document (PDF)

Title: CHARACTERIZATION OF DIFFERENTIATED HUMAN NEUROBLASTOMA SH-SY5Y CELLS IN CULTURE.
Creator: Condikey, Siri, Prentice, Howard, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
Abstract/Description: Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases affecting an estimated 20 million worldwide. The primary pathology of AD is the progressive loss of basal forebrain cholinergic neurons, which is responsible for the cognitive decline experienced by AD patients. The mechanisms underlying this selective vulnerability have not been fully elucidated. Furthermore, oxidative stress is a key factor behind the pathology of AD leading to this neuronal loss. The current...
Show moreAlzheimer’s disease (AD) is one of the most common neurodegenerative diseases affecting an estimated 20 million worldwide. The primary pathology of AD is the progressive loss of basal forebrain cholinergic neurons, which is responsible for the cognitive decline experienced by AD patients. The mechanisms underlying this selective vulnerability have not been fully elucidated. Furthermore, oxidative stress is a key factor behind the pathology of AD leading to this neuronal loss. The current literature suggests that there are limited in-vitro models available to accurately simulate the hallmark symptoms of Alzheimer's disease (AD). The SH-SY5Y cell line has been used extensively to study neuronal stress responses but the undifferentiated cell type has been predominantly used. Undifferentiated SH-SY5Y versus differentiated SH-SY5Y have been shown to have different interaction, expression and localization with AD hallmark, amyloid-b -42. This project sought to use differentiated cholinergic cells from the line SH-SY5Y to further isolate and elucidate, in-vitro, the mechanisms behind the oxidative stress response, a key stressor in the pathology of AD. Building upon previous studies, a protocol to differentiate SH-SY5Y cells with retinoic acid (RA) and neurotrophin (BDNF) to mature neurons of the cholinergic phenotype was optimized and implemented. The results showed successful differentiation into the cholinergic phenotype as evidenced via immunofluorescence imaging of choline acetyl transferase (ChAT) expression and mature neurite morphology. To simulate oxidative stress, we exposed both undifferentiated and differentiated SH-SY5Y cells to hypoxic conditions. Results indicated a stress response to mild hypoxic conditions with higher sensitivity in cholinergic differentiated SH-SY5Y. Understanding these hallmark mechanisms behind oxidative stress is crucial to developing mechanism-based therapeutics for AD.
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Date Issued: 2023
PURL: http://purl.flvc.org/fau/fd/FA00014347
Subject Headings: Alzheimer Disease, Cholinergic Neurons, Alzheimer Disease--pathology
Format: Document (PDF)

Title: Pharmacological protection of retinal pigmented epithelial cells by sulindac involves PPAR-α.
Creator: Sur, Arunodoy, Kesaraju, Shailaja, Prentice, Howard, Ayyanathan, Kasirajan, Baronas-Lowell, Diane, Zhu, Danhong, Hinton, David R., Blanks, Janet, Weissbach, Herbert
Date Issued: 2014-11-10
PURL: http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1073_pnas.1419576111_1631807081
Format: Citation

Title: Mechanisms of Neuronal Protection against Excitotoxicity, Endoplasmic Reticulum Stress, and Mitochondrial Dysfunction in Stroke and Neurodegenerative Diseases.
Creator: Prentice, Howard, Modi, Jigar P., Wu, Jang-Yen
Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FAUIR000111
Format: Citation

FAU College Collections (6)	+ -
FAU Theses and Dissertations (6)	+ -
FAU Graduate Student Research (3)	+ -
Florida Atlantic University Patents (3)	+ -
FAU Undergraduate Student Research (1)	+ -

Taurine (3)	+ -
Alzheimer Disease (2)	+ -
Gene therapy (2)	+ -
Alzheimer Disease--pathology (1)	+ -
Antioxidants --pharmacology (1)	+ -

Apoptosis (1)	+ -
Apoptosis Regulatory Proteins (1)	+ -
Cell differentiation (1)	+ -
Cellular signal transduction (1)	+ -
Central Nervous System --metabolism (1)	+ -
Cholinergic Neurons (1)	+ -
Decorin (1)	+ -
Endoplasmic Reticulum --drug effects (1)	+ -
Endoplasmic reticulum (1)	+ -
Epithelial cells (1)	+ -
GABA --physiology (1)	+ -
Gamma-aminoboterzuur (1)	+ -
Genetic Therapy (1)	+ -
Glutamates (1)	+ -
Glutamic Acid --metabolism (1)	+ -
Granulocyte Colony-Stimulating Factor (1)	+ -
Granulocyte-colony stimulating factor (1)	+ -
Heart--Pathophysiology (1)	+ -
Homeostasis --physiology (1)	+ -
Macular Degeneration (1)	+ -
Mitochondrial pathology (1)	+ -
Nervous System Diseases (1)	+ -
Neuroprotective Agents (1)	+ -
Neuroprotective Agents --metabolism (1)	+ -
Neurotransmitter Agents (1)	+ -

Electronic Thesis or Dissertation (6)	+ -
abstract (3)	+ -
article (3)	+ -
patent (3)	+ -
poster (1)	+ -

Prentice, Howard (18)	+ -
Florida Atlantic University (9)	+ -
Wu, Jang-Yen (7)	+ -
Blanks, Janet C. (4)	+ -
Pan, Chunliu (4)	+ -

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