The Experts below are selected from a list of 5235 Experts worldwide ranked by ideXlab platform
A Giovanni - One of the best experts on this subject based on the ideXlab platform.
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guanosine 3 5 cyclic monophosphate mediated inhibition of Cell death induced by nerve growth factor withdrawal and β amyloid protective effects of propentofylline
Neuroscience, 2000Co-Authors: F Wirtzbrugger, A GiovanniAbstract:Abstract Apoptotic Cell death has been implicated in Alzheimer’s disease pathology and amyloid peptide induced neurotoxicity. We investigated the survival promoting effects of Propentofylline in two models of apoptotic Cell death, nerve growth factor withdrawal and β-amyloid mediated Cell death in nerve growth factor differentiated rat Pheochromocytoma Cell lines. The increase in Cell death as measured by lactate dehydrogenase release in response to nerve growth factor withdrawal was suppressed by nitric oxide donor S -nitroso- N -acetylpenicillamine (12.5 to 200 μM) and by 8-bromoguanosine-3′,5′-cyclic monophosphate (1.25 to 10 mM). Both agents decreased Cell death mediated by 25 μM β-amyloid, suggesting that the protective mechanism involves guanosine -3′,5′-cyclic monophosphate. In support of this hypothesis we can show that S -nitroso- N -acetylpenicillamine increases intraCellular levels of guanosine -3′,5′-cyclic monophosphate in Pheochromocytoma Cell lines 3 to 8 fold. Propentofylline, a phosphodiesterase inhibitor, has previously demonstrated neuroprotective activity in stroke models and is a potential candidate for therapeutic treatment in neurodegenerative diseases. The present findings support this claim by providing evidence that Propentofylline has protective effects in both nerve growth factor withdrawal and β-amyloid mediated Cell death. Lactate dehydrogenase release was significantly reduced and caspase-3-like activity was attenuated after cotreatment with Propentofylline. Furthermore Propentofylline dose responsively increases intraCellular guanosine-3′,5′-cyclic monophosphate levels over the same dose range that provided protection. We hypothesized that guanosine-3′,5′-cyclic monophosphate is a key mediator of neuroprotection under these conditions.
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guanosine 3 5 cyclic monophosphate mediated inhibition of Cell death induced by nerve growth factor withdrawal and β amyloid protective effects of propentofylline
Neuroscience, 2000Co-Authors: F Wirtzbrugger, A GiovanniAbstract:Apoptotic Cell death has been implicated in Alzheimer's disease pathology and amyloid peptide induced neurotoxicity. We investigated the survival promoting effects of Propentofylline in two models of apoptotic Cell death, nerve growth factor withdrawal and beta-amyloid mediated Cell death in nerve growth factor differentiated rat Pheochromocytoma Cell lines. The increase in Cell death as measured by lactate dehydrogenase release in response to nerve growth factor withdrawal was suppressed by nitric oxide donor S-nitroso-N-acetylpenicillamine (12.5 to 200 microM) and by 8-bromoguanosine-3',5'-cyclic monophosphate (1.25 to 10mM). Both agents decreased Cell death mediated by 25 microM beta-amyloid, suggesting that the protective mechanism involves guanosine -3', 5'-cyclic monophosphate. In support of this hypothesis we can show that S-nitroso-N-acetylpenicillamine increases intraCellular levels of guanosine -3',5'-cyclic monophosphate in Pheochromocytoma Cell lines 3 to 8 fold.Propentofylline, a phosphodiesterase inhibitor, has previously demonstrated neuroprotective activity in stroke models and is a potential candidate for therapeutic treatment in neurodegenerative diseases. The present findings support this claim by providing evidence that Propentofylline has protective effects in both nerve growth factor withdrawal and beta-amyloid mediated Cell death. Lactate dehydrogenase release was significantly reduced and caspase-3-like activity was attenuated after cotreatment with Propentofylline. Furthermore Propentofylline dose responsively increases intraCellular guanosine-3',5'-cyclic monophosphate levels over the same dose range that provided protection. We hypothesized that guanosine-3',5'-cyclic monophosphate is a key mediator of neuroprotection under these conditions.
F Wirtzbrugger - One of the best experts on this subject based on the ideXlab platform.
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guanosine 3 5 cyclic monophosphate mediated inhibition of Cell death induced by nerve growth factor withdrawal and β amyloid protective effects of propentofylline
Neuroscience, 2000Co-Authors: F Wirtzbrugger, A GiovanniAbstract:Abstract Apoptotic Cell death has been implicated in Alzheimer’s disease pathology and amyloid peptide induced neurotoxicity. We investigated the survival promoting effects of Propentofylline in two models of apoptotic Cell death, nerve growth factor withdrawal and β-amyloid mediated Cell death in nerve growth factor differentiated rat Pheochromocytoma Cell lines. The increase in Cell death as measured by lactate dehydrogenase release in response to nerve growth factor withdrawal was suppressed by nitric oxide donor S -nitroso- N -acetylpenicillamine (12.5 to 200 μM) and by 8-bromoguanosine-3′,5′-cyclic monophosphate (1.25 to 10 mM). Both agents decreased Cell death mediated by 25 μM β-amyloid, suggesting that the protective mechanism involves guanosine -3′,5′-cyclic monophosphate. In support of this hypothesis we can show that S -nitroso- N -acetylpenicillamine increases intraCellular levels of guanosine -3′,5′-cyclic monophosphate in Pheochromocytoma Cell lines 3 to 8 fold. Propentofylline, a phosphodiesterase inhibitor, has previously demonstrated neuroprotective activity in stroke models and is a potential candidate for therapeutic treatment in neurodegenerative diseases. The present findings support this claim by providing evidence that Propentofylline has protective effects in both nerve growth factor withdrawal and β-amyloid mediated Cell death. Lactate dehydrogenase release was significantly reduced and caspase-3-like activity was attenuated after cotreatment with Propentofylline. Furthermore Propentofylline dose responsively increases intraCellular guanosine-3′,5′-cyclic monophosphate levels over the same dose range that provided protection. We hypothesized that guanosine-3′,5′-cyclic monophosphate is a key mediator of neuroprotection under these conditions.
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guanosine 3 5 cyclic monophosphate mediated inhibition of Cell death induced by nerve growth factor withdrawal and β amyloid protective effects of propentofylline
Neuroscience, 2000Co-Authors: F Wirtzbrugger, A GiovanniAbstract:Apoptotic Cell death has been implicated in Alzheimer's disease pathology and amyloid peptide induced neurotoxicity. We investigated the survival promoting effects of Propentofylline in two models of apoptotic Cell death, nerve growth factor withdrawal and beta-amyloid mediated Cell death in nerve growth factor differentiated rat Pheochromocytoma Cell lines. The increase in Cell death as measured by lactate dehydrogenase release in response to nerve growth factor withdrawal was suppressed by nitric oxide donor S-nitroso-N-acetylpenicillamine (12.5 to 200 microM) and by 8-bromoguanosine-3',5'-cyclic monophosphate (1.25 to 10mM). Both agents decreased Cell death mediated by 25 microM beta-amyloid, suggesting that the protective mechanism involves guanosine -3', 5'-cyclic monophosphate. In support of this hypothesis we can show that S-nitroso-N-acetylpenicillamine increases intraCellular levels of guanosine -3',5'-cyclic monophosphate in Pheochromocytoma Cell lines 3 to 8 fold.Propentofylline, a phosphodiesterase inhibitor, has previously demonstrated neuroprotective activity in stroke models and is a potential candidate for therapeutic treatment in neurodegenerative diseases. The present findings support this claim by providing evidence that Propentofylline has protective effects in both nerve growth factor withdrawal and beta-amyloid mediated Cell death. Lactate dehydrogenase release was significantly reduced and caspase-3-like activity was attenuated after cotreatment with Propentofylline. Furthermore Propentofylline dose responsively increases intraCellular guanosine-3',5'-cyclic monophosphate levels over the same dose range that provided protection. We hypothesized that guanosine-3',5'-cyclic monophosphate is a key mediator of neuroprotection under these conditions.
Arthur S Tischler - One of the best experts on this subject based on the ideXlab platform.
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microarray based comparative genomic hybridization of Pheochromocytoma Cell lines from neurofibromatosis knockout mice reveals genetic alterations similar to those in human Pheochromocytomas
Cancer Genetics and Cytogenetics, 2005Co-Authors: James F Powers, Arthur S Tischler, Mansoor Mohammed, Rizwann NaeemAbstract:Somatic genetic aberrations have been identified in both sporadic Pheochromocytomas and those associated with familial tumor syndromes; however, individual variations between human tumors and the absence of in vitro human Pheochromocytoma models hinder efforts to understand the roles of those aberrations in tumorigenesis. Pheochromocytomas occur frequently in neurofibromatosis knockout mice and we have recently developed Cell lines from those tumors. The availability of multiple tumors from genetically identical animals provides a powerful tool for understanding the pathobiology of Pheochromocytomas. For the present investigation, we performed a genomic scanning analysis of four mouse Pheochromocytoma Cell lines by standard cytogenetics and microarray-based comparative genomic hybridization in order to identify genetic common denominators. All of the lines showed losses of most or all of chromosome 9; three lines lost most or all of chromosome 4. Mouse chromosome 4 is homologous to human chromosome 1p, which is the most frequent deletion in human Pheochromocytomas. Mouse chromosome 9 shows large areas of homology to human 3p, 3q, and 11q, which are also frequently deleted. These comparisons suggest that genetic mechanisms in the genesis of Pheochromocytomas may be similar across species. Additional changes that may be specific to this model included complete or partial gains of chromosome 12 as seen in 3 of the 4 lines analyzed by array CGH.
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expression of recombinant calcium channels support secretion in a mouse Pheochromocytoma Cell line
Journal of Neurophysiology, 2003Co-Authors: Amy B Harkins, Anne L Cahill, James F Powers, Arthur S Tischler, Aaron P FoxAbstract:We have characterized a recently established mouse Pheochromocytoma Cell line (MPC 9/3L) as a useful model for studying neurotransmitter release and neuroendocrine secretion. MPC 9/3L Cells express...
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plasticity of Pheochromocytoma Cell lines from neurofibromatosis knockout mice
Annals of the New York Academy of Sciences, 2002Co-Authors: James F Powers, Kimberley Schelling, Jaime M Brachold, Arthur S TischlerAbstract:Adrenergic mouse Pheochromocytoma (MPC) Cells from heterozygous neurofibromatosis knockout mice show little or no expression of the NGF receptor trk A and do not undergo neuronal differentiation in response to NGF. However, they express high levels of receptor tyrosine kinase, Ret, and GDNF family receptor alpha(1) (GFRalpha(1)) in vivo and in vitro and respond to glial Cell line-derived neurotrophic factor (GDNF). In addition, they form short processes in response to PACAP or cyclic AMP. Morphological effects of GDNF, PACAP, or cyclic AMP are similar to those of NGF, PACAP, or cyclic AMP on PC12 Cells, and all three agents cause downregulation of PNMT mRNA. The MAP kinase kinase inhibitor U0126 inhibits both baseline proliferation and stimulated process outgrowth, consistent with a model in which sustained low-level ERK activation drives proliferation, and more intense activation drives neuronal differentiation. The sensitivity of MPC Cells to U0126 both may reflect mechanisms that cause Pheochromocytomas in neurofibromatosis and aid in their clarification.
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high level expression of receptor tyrosine kinase ret and responsiveness to ret activating ligands in Pheochromocytoma Cell lines from neurofibromatosis knockout mice
Molecular and Cellular Neuroscience, 2002Co-Authors: James F Powers, Kimberley Schelling, Jaime M Brachold, Panayiotis Tsokas, Hagit Schayek, Eitan Friedman, Arthur S TischlerAbstract:Pheochromocytoma Cell lines derived from neurofibromatosis knockout mice express high levels of the receptor tyrosine kinase Ret, which is involved in the pathogenesis of human Pheochromocytomas in hereditary multiple endocrine neoplasia syndrome type 2 (MEN2). Mouse Pheochromocytoma (MPC) Cells respond to the Ret-activating ligand GDNF by exhibiting Ret phosphorylation, neurite outgrowth, decreased proliferation, and altered expression of catecholamine biosynthetic enzymes. GDNF exerts similar effects on human Pheochromocytoma Cells in primary cultures. Ret is minimally expressed by normal mouse chromaffin Cells, from which Pheochromocytomas are derived. Its expression at high levels by MPC Cells suggests possible relationships between two previously unrelated tumor syndromes, neurofibromatosis, and MEN2. The responsiveness of these Cells to GDNF suggests that they may be a valuable new model for neurobiology.
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Pheochromocytoma Cell lines from heterozygous neurofibromatosis knockout mice
Cell and Tissue Research, 2000Co-Authors: James F Powers, Panayiotis Tsokas, Marian J Evinger, Shahinaz Bedri, Joseph Alroy, Mohsen Shahsavari, Arthur S TischlerAbstract:Transplantable tumors and Cell lines have been developed from Pheochromocytomas arising in mice with a heterozygous knockout mutation of the neurofibromatosis gene, Nf1. Nf1 encodes a ras-GTPase-activating protein, neurofibromin, and mouse Pheochromocytoma (MPC) Cells in primary cultures typically show extensive spontaneous neuronal differentiation that may result from the loss of the remaining wild-type allele and defective regulation of ras signaling. However, all MPC Cell lines express neurofibromin, suggesting that preservation of the wild-type allele may be required to permit the propagation of MPC Cells in vitro. MPC lines differ from PC12 Cells in that they express both endogenous phenylethanolamine N-methyltransferase (PNMT) and full-length PNMT reporter constructs. PNMT expression is increased by dexamethasone and by Cell-Cell contact in suspension cultures. Mouse Pheochromocytomas are a new tool for studying genes and signaling pathways that regulate Cell growth and differentiation in adrenal medullary neoplasms and are a unique model for studying the regulation of PNMT expression.
Ruilin Shen - One of the best experts on this subject based on the ideXlab platform.
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apocynin attenuates cobalt chloride induced Pheochromocytoma Cell apoptosis by inhibiting p38 mapk caspase 3 pathway
Cellular Physiology and Biochemistry, 2018Co-Authors: Jie Liu, Yuzhang Zhu, Shipiao Chen, Bin Shen, Yi Zhang, Ruilin ShenAbstract:Background/aims Apocynin, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, has been identified as a potential neuroprotectant. In this study, we aimed to investigate the protective effect of apocynin against cobalt chloride (CoCl2)-induced Pheochromocytoma (PC12) Cell apoptosis. Methods The PC12 Cell culture was pretreated with apocynin and/or SB203580 (p38 mitogen-activated protein kinase [p38-MAPK] inhibitor) at different time points prior to CoCl2 incubation. The Cell viability, apoptosis rate, DAN damage, and antioxidant activity were detected using Cell counting kit-8 (CCK-8), flow cytometry, enzyme-linked immunosorbent assay (ELISA), and comet assay respectively. The protein and mRNA expressions of p38-MAPK and caspase-3 in the Cells were measured by qRT-PCR and Western blotting. Results Apocynin inhibited CoCl2-mediated apoptosis, reduced oxidative stress, and down-regulated the expression of p38-MAPK and caspase-3. Conclusions Our findings show that apocynin attenuated CoCl2-induced apoptosis by potently restraining p38-MAPK-caspase-3 signaling pathway in PC12 Cells, suggesting that apocynin may be a potent prophylactic reagent against CoCl2-mediated PC12 Cell apoptosis.
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Apocynin Attenuates Cobalt Chloride-Induced Pheochromocytoma Cell Apoptosis by Inhibiting P38-MAPK/Caspase-3 Pathway
Karger Publishers, 2018Co-Authors: Jie Liu, Yuzhang Zhu, Shipiao Chen, Bin Shen, Yi Zhang, Ruilin ShenAbstract:Background/Aims: Apocynin, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, has been identified as a potential neuroprotectant. In this study, we aimed to investigate the protective effect of apocynin against cobalt chloride (CoCl2)-induced Pheochromocytoma (PC12) Cell apoptosis. Methods: The PC12 Cell culture was pretreated with apocynin and/or SB203580 (p38 mitogen-activated protein kinase [p38-MAPK] inhibitor) at different time points prior to CoCl2 incubation. The Cell viability, apoptosis rate, DAN damage, and antioxidant activity were detected using Cell counting kit-8 (CCK-8), flow cytometry, enzyme-linked immunosorbent assay (ELISA), and comet assay respectively. The protein and mRNA expressions of p38-MAPK and caspase-3 in the Cells were measured by qRT-PCR and Western blotting. Results: Apocynin inhibited CoCl2-mediated apoptosis, reduced oxidative stress, and down-regulated the expression of p38-MAPK and caspase-3. Conclusions: Our findings show that apocynin attenuated CoCl2-induced apoptosis by potently restraining p38-MAPK-caspase-3 signaling pathway in PC12 Cells, suggesting that apocynin may be a potent prophylactic reagent against CoCl2-mediated PC12 Cell apoptosis
Susana Nowicki - One of the best experts on this subject based on the ideXlab platform.
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cytochrome 450 metabolites of arachidonic acid 20 hete 11 12 eet and 14 15 eet promote Pheochromocytoma Cell growth and tumor associated angiogenesis
Biochimie, 2020Co-Authors: Cecilia Colombero, Sofia Cardenas, Marcela Venara, Ayelen Martin, Patricia Pennisi, Marta Barontini, Susana NowickiAbstract:Abstract The importance of cytochrome P450 (CYP)-derived arachidonic acid (AA) metabolites, 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs) as tumor growth promotors has already been described in several cancer types. The aim of this study was to evaluate the role of these compounds in the biology of Pheochromocytoma/paraganglioma. These tumors originate from chromaffin Cells derived from adrenal medulla (Pheochromocytomas) or extra-adrenal autonomic paraganglia (paragangliomas), and they represent the most common hereditary endocrine neoplasia. According to mutations in the driver genes, these tumors are divided in two clusters: pseudo-hypoxic and kinase-signaling EETs, but not 20-HETE, exhibited a potent ability to sustain growth in a murine Pheochromocytoma Cell line (MPC) in vitro, EETs promoted an increase in Cell proliferation and a decrease in Cell apoptosis. In a mouse model of Pheochromocytoma, the inhibition of CYP-mediated AA metabolism using 1-aminobenzotriazol resulted in slower tumor growth, a decreased vascularization, and a lower final volume. Also, the expression of AA-metabolizing CYP monooxygenases was detected in tumor samples from human origin, being their apparent abundance and the production of both metabolites higher in tumors from the kinase-signaling cluster. This is the first evidence of the importance of CYP- derived AA metabolites in the biology and development of Pheochromocytoma/paraganglioma tumors.
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igf i regulates Pheochromocytoma Cell proliferation and survival in vitro and in vivo
Endocrinology, 2012Co-Authors: Maria Celia Fernandez, Marcela Venara, Marta Barontini, Susana Nowicki, H E Chemes, Patricia PennisiAbstract:IGFs are involved in malignant transformation and growth of several tissues, including the adrenal medulla. The present study was designed to evaluate the impact of IGF-I on Pheochromocytoma development. We used a murine Pheochromocytoma (MPC) Cell line (MPC4/30) and an animal model with a reduction of 75% in circulating IGF-I levels [liver-IGF-I-deficient (LID) mice] to perform studies in vitro and in vivo. We found that, in culture, IGF-I stimulation increases proliferation, migration, and anchorage-independent growth, whereas it inhibits apoptosis of MPC Cells. When injected to control and to LID mice, MPC Cells grow and form tumors with features of Pheochromocytoma. Six weeks after Cell inoculation, all control mice developed sc tumors. In contrast, in 73% of LID mice, tumor development was delayed to 7–12 wk, and the remaining 27% did not develop tumors up to 12 wk after inoculation. LID mice harboring MPC Cells and treated with recombinant human IGF-I (LID+) developed tumors as controls. Tumors deve...