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Julie Gehl - One of the best experts on this subject based on the ideXlab platform.
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difference in membrane repair capacity between cancer Cell Lines and a normal Cell Line
The Journal of Membrane Biology, 2016Co-Authors: Stine Krog Frandsen, Anna K Mcneil, Ivana Novak, Paul L Mcneil, Julie GehlAbstract:Electroporation-based treatments and other therapies that permeabilize the plasma membrane have been shown to be more devastating to malignant Cells than to normal Cells. In this study, we asked if a difference in repair capacity could explain this observed difference in sensitivity. Membrane repair was investigated by disrupting the plasma membrane using laser followed by monitoring fluorescent dye entry over time in seven cancer Cell Lines, an Immortalized Cell Line, and a normal primary Cell Line. The kinetics of repair in living Cells can be directly recorded using this technique, providing a sensitive index of repair capacity. The normal primary Cell Line of all tested Cell Lines exhibited the slowest rate of dye entry after laser disruption and lowest level of dye uptake. Significantly, more rapid dye uptake and a higher total level of dye uptake occurred in six of the seven tested cancer Cell Lines (p < 0.05) as well as the Immortalized Cell Line (p < 0.001). This difference in sensitivity was also observed when a viability assay was performed one day after plasma membrane permeabilization by electroporation. Viability in the primary normal Cell Line (98 % viable Cells) was higher than in the three tested cancer Cell Lines (81–88 % viable Cells). These data suggest more effective membrane repair in normal, primary Cells and supplement previous explanations why electroporation-based therapies and other therapies permeabilizing the plasma membrane are more effective on malignant Cells compared to normal Cells in cancer treatment.
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Difference in Membrane Repair Capacity Between Cancer Cell Lines and a Normal Cell Line
The Journal of membrane biology, 2016Co-Authors: Stine Krog Frandsen, Anna K Mcneil, Ivana Novak, Paul L Mcneil, Julie GehlAbstract:Electroporation-based treatments and other therapies that permeabilize the plasma membrane have been shown to be more devastating to malignant Cells than to normal Cells. In this study, we asked if a difference in repair capacity could explain this observed difference in sensitivity. Membrane repair was investigated by disrupting the plasma membrane using laser followed by monitoring fluorescent dye entry over time in seven cancer Cell Lines, an Immortalized Cell Line, and a normal primary Cell Line. The kinetics of repair in living Cells can be directly recorded using this technique, providing a sensitive index of repair capacity. The normal primary Cell Line of all tested Cell Lines exhibited the slowest rate of dye entry after laser disruption and lowest level of dye uptake. Significantly, more rapid dye uptake and a higher total level of dye uptake occurred in six of the seven tested cancer Cell Lines (p
Pablo Caviedes - One of the best experts on this subject based on the ideXlab platform.
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Knockdown of Myo-Inositol Transporter SMIT1 Normalizes ChoLinergic and Glutamatergic Function in an Immortalized Cell Line Established from the Cerebral Cortex of a Trisomy 16 Fetal Mouse, an Animal Model of Human Trisomy 21 (Down Syndrome)
Neurotoxicity Research, 2017Co-Authors: Ana María Cárdenas, Paola Fernández-olivares, Ignacio Díaz-franulic, Arlek M. González-jamett, Takeshi Shimahara, Juan Segura-aguilar, Raúl Caviedes, Pablo CaviedesAbstract:The Na^+/myo-inositol cotransporter (SMIT1) is overexpressed in human Down syndrome (DS) and in trisomy 16 fetal mice (Ts16), an animal model of the human condition. SMIT1 overexpression determines increased levels of intraCellular myo-inositol, a precursor of phophoinositide synthesis. SMIT1 is overexpressed in CTb Cells, an Immortalized Cell Line established from the cerebral cortex of a Ts16 mouse fetus. CTb Cells exhibit impaired cytosolic Ca^2+ signals in response to glutamatergic and choLinergic stimuli (increased amplitude and delayed time-dependent kinetics in the decay post-stimulation), compared to our CNh Cell Line, derived from the cerebral cortex of a euploid animal. Considering the role of myo-inositol in intraCellular signaling, we normalized SMIT1 expression in CTb Cells using specific mRNA antisenses. Forty-eight hours post-transfection, SMIT1 levels in CTb Cells reached values comparable to those of CNh Cells. At this time, decay kinetics of Ca^2+ signals induced by either glutamate, nicotine, or muscarine were accelerated in transfected CTb Cells, to values similar to those of CNh Cells. The amplitude of glutamate-induced cytosolic Ca^2+ signals in CTb Cells was also normalized. The results suggest that SMIT1 overexpression contributes to abnormal choLinergic and glutamatergic Ca^2+ signals in the trisomic condition, and knockdown of DS-related genes in our Ts16-derived Cell Line could constitute a relevant tool to study DS-related neuronal dysfunction.
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Small-molecule aggregation inhibitors reduce excess amyloid in a trisomy 16 mouse cortical Cell Line
Biological Research, 2008Co-Authors: Andréa C. Paula Lima, Raúl Caviedes, Pablo Caviedes, Christian Arriagada, Rodrigo Toro, Ana M. Cárdenas, Sergio T. FerreiraAbstract:We have previously characterized a number of small molecule organic compounds that prevent the aggregation of the β-amyloid peptide and its neurotoxicity in hippocampal neuronal cultures. We have now evaluated the effects of such compounds on amyloid precursor protein (APP) accumulation in the CTb Immortalized Cell Line derived from the cerebral cortex of a trisomy 16 mouse, an animal model of Down’s syndrome. Compared to a non-trisomic cortical Cell Line (CNh), CTb Cells overexpress APP and exhibit slightly elevated resting intraCellular Ca 2+ levels ([Ca 2+ ] i ). Here, we show that the compounds 2,4dinitrophenol, 3-nitrophenol and 4-anisidine decreased intraCellular accumulation of APP in CTb Cells. Those compounds were non-toxic to the Cells, and slightly increased the basal [Ca 2+ ] i . Results indicate that the compounds tested can be leads for the development of drugs to decrease intraCellular vesicular accumulation of APP in trisomic Cells. Key terms: Alzheimer’s disease, Down syndrome, intraCellular amyloid, murine trisomy 16, small molecule inhibitors.
Stine Krog Frandsen - One of the best experts on this subject based on the ideXlab platform.
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difference in membrane repair capacity between cancer Cell Lines and a normal Cell Line
The Journal of Membrane Biology, 2016Co-Authors: Stine Krog Frandsen, Anna K Mcneil, Ivana Novak, Paul L Mcneil, Julie GehlAbstract:Electroporation-based treatments and other therapies that permeabilize the plasma membrane have been shown to be more devastating to malignant Cells than to normal Cells. In this study, we asked if a difference in repair capacity could explain this observed difference in sensitivity. Membrane repair was investigated by disrupting the plasma membrane using laser followed by monitoring fluorescent dye entry over time in seven cancer Cell Lines, an Immortalized Cell Line, and a normal primary Cell Line. The kinetics of repair in living Cells can be directly recorded using this technique, providing a sensitive index of repair capacity. The normal primary Cell Line of all tested Cell Lines exhibited the slowest rate of dye entry after laser disruption and lowest level of dye uptake. Significantly, more rapid dye uptake and a higher total level of dye uptake occurred in six of the seven tested cancer Cell Lines (p < 0.05) as well as the Immortalized Cell Line (p < 0.001). This difference in sensitivity was also observed when a viability assay was performed one day after plasma membrane permeabilization by electroporation. Viability in the primary normal Cell Line (98 % viable Cells) was higher than in the three tested cancer Cell Lines (81–88 % viable Cells). These data suggest more effective membrane repair in normal, primary Cells and supplement previous explanations why electroporation-based therapies and other therapies permeabilizing the plasma membrane are more effective on malignant Cells compared to normal Cells in cancer treatment.
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Difference in Membrane Repair Capacity Between Cancer Cell Lines and a Normal Cell Line
The Journal of membrane biology, 2016Co-Authors: Stine Krog Frandsen, Anna K Mcneil, Ivana Novak, Paul L Mcneil, Julie GehlAbstract:Electroporation-based treatments and other therapies that permeabilize the plasma membrane have been shown to be more devastating to malignant Cells than to normal Cells. In this study, we asked if a difference in repair capacity could explain this observed difference in sensitivity. Membrane repair was investigated by disrupting the plasma membrane using laser followed by monitoring fluorescent dye entry over time in seven cancer Cell Lines, an Immortalized Cell Line, and a normal primary Cell Line. The kinetics of repair in living Cells can be directly recorded using this technique, providing a sensitive index of repair capacity. The normal primary Cell Line of all tested Cell Lines exhibited the slowest rate of dye entry after laser disruption and lowest level of dye uptake. Significantly, more rapid dye uptake and a higher total level of dye uptake occurred in six of the seven tested cancer Cell Lines (p
Paul L Mcneil - One of the best experts on this subject based on the ideXlab platform.
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difference in membrane repair capacity between cancer Cell Lines and a normal Cell Line
The Journal of Membrane Biology, 2016Co-Authors: Stine Krog Frandsen, Anna K Mcneil, Ivana Novak, Paul L Mcneil, Julie GehlAbstract:Electroporation-based treatments and other therapies that permeabilize the plasma membrane have been shown to be more devastating to malignant Cells than to normal Cells. In this study, we asked if a difference in repair capacity could explain this observed difference in sensitivity. Membrane repair was investigated by disrupting the plasma membrane using laser followed by monitoring fluorescent dye entry over time in seven cancer Cell Lines, an Immortalized Cell Line, and a normal primary Cell Line. The kinetics of repair in living Cells can be directly recorded using this technique, providing a sensitive index of repair capacity. The normal primary Cell Line of all tested Cell Lines exhibited the slowest rate of dye entry after laser disruption and lowest level of dye uptake. Significantly, more rapid dye uptake and a higher total level of dye uptake occurred in six of the seven tested cancer Cell Lines (p < 0.05) as well as the Immortalized Cell Line (p < 0.001). This difference in sensitivity was also observed when a viability assay was performed one day after plasma membrane permeabilization by electroporation. Viability in the primary normal Cell Line (98 % viable Cells) was higher than in the three tested cancer Cell Lines (81–88 % viable Cells). These data suggest more effective membrane repair in normal, primary Cells and supplement previous explanations why electroporation-based therapies and other therapies permeabilizing the plasma membrane are more effective on malignant Cells compared to normal Cells in cancer treatment.
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Difference in Membrane Repair Capacity Between Cancer Cell Lines and a Normal Cell Line
The Journal of membrane biology, 2016Co-Authors: Stine Krog Frandsen, Anna K Mcneil, Ivana Novak, Paul L Mcneil, Julie GehlAbstract:Electroporation-based treatments and other therapies that permeabilize the plasma membrane have been shown to be more devastating to malignant Cells than to normal Cells. In this study, we asked if a difference in repair capacity could explain this observed difference in sensitivity. Membrane repair was investigated by disrupting the plasma membrane using laser followed by monitoring fluorescent dye entry over time in seven cancer Cell Lines, an Immortalized Cell Line, and a normal primary Cell Line. The kinetics of repair in living Cells can be directly recorded using this technique, providing a sensitive index of repair capacity. The normal primary Cell Line of all tested Cell Lines exhibited the slowest rate of dye entry after laser disruption and lowest level of dye uptake. Significantly, more rapid dye uptake and a higher total level of dye uptake occurred in six of the seven tested cancer Cell Lines (p
Anna K Mcneil - One of the best experts on this subject based on the ideXlab platform.
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difference in membrane repair capacity between cancer Cell Lines and a normal Cell Line
The Journal of Membrane Biology, 2016Co-Authors: Stine Krog Frandsen, Anna K Mcneil, Ivana Novak, Paul L Mcneil, Julie GehlAbstract:Electroporation-based treatments and other therapies that permeabilize the plasma membrane have been shown to be more devastating to malignant Cells than to normal Cells. In this study, we asked if a difference in repair capacity could explain this observed difference in sensitivity. Membrane repair was investigated by disrupting the plasma membrane using laser followed by monitoring fluorescent dye entry over time in seven cancer Cell Lines, an Immortalized Cell Line, and a normal primary Cell Line. The kinetics of repair in living Cells can be directly recorded using this technique, providing a sensitive index of repair capacity. The normal primary Cell Line of all tested Cell Lines exhibited the slowest rate of dye entry after laser disruption and lowest level of dye uptake. Significantly, more rapid dye uptake and a higher total level of dye uptake occurred in six of the seven tested cancer Cell Lines (p < 0.05) as well as the Immortalized Cell Line (p < 0.001). This difference in sensitivity was also observed when a viability assay was performed one day after plasma membrane permeabilization by electroporation. Viability in the primary normal Cell Line (98 % viable Cells) was higher than in the three tested cancer Cell Lines (81–88 % viable Cells). These data suggest more effective membrane repair in normal, primary Cells and supplement previous explanations why electroporation-based therapies and other therapies permeabilizing the plasma membrane are more effective on malignant Cells compared to normal Cells in cancer treatment.
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Difference in Membrane Repair Capacity Between Cancer Cell Lines and a Normal Cell Line
The Journal of membrane biology, 2016Co-Authors: Stine Krog Frandsen, Anna K Mcneil, Ivana Novak, Paul L Mcneil, Julie GehlAbstract:Electroporation-based treatments and other therapies that permeabilize the plasma membrane have been shown to be more devastating to malignant Cells than to normal Cells. In this study, we asked if a difference in repair capacity could explain this observed difference in sensitivity. Membrane repair was investigated by disrupting the plasma membrane using laser followed by monitoring fluorescent dye entry over time in seven cancer Cell Lines, an Immortalized Cell Line, and a normal primary Cell Line. The kinetics of repair in living Cells can be directly recorded using this technique, providing a sensitive index of repair capacity. The normal primary Cell Line of all tested Cell Lines exhibited the slowest rate of dye entry after laser disruption and lowest level of dye uptake. Significantly, more rapid dye uptake and a higher total level of dye uptake occurred in six of the seven tested cancer Cell Lines (p
