The Experts below are selected from a list of 209031 Experts worldwide ranked by ideXlab platform
Kathy K Griendling - One of the best experts on this subject based on the ideXlab platform.
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p38 mitogen activated protein kinase is a Critical Component of the redox sensitive signaling pathways activated by angiotensin ii role in vascular smooth muscle cell hypertrophy
Journal of Biological Chemistry, 1998Co-Authors: Masuko Ushiofukai, Wayne R Alexander, M Akers, Kathy K GriendlingAbstract:Abstract Angiotensin II induces an oxidant stress-dependent hypertrophy in cultured vascular smooth muscle cells. To investigate the growth-related molecular targets of H2O2, we examined the redox sensitivity of agonist-stimulated activation of the mitogen-activated protein kinase (MAPK) family. We show here that angiotensin II elicits a rapid increase in intracellular H2O2 and a rapid and robust phosphorylation of both p42/44MAPK (16-fold) and p38MAPK (15-fold). However, exogenous H2O2 activates only p38MAPK (14-fold), and diphenylene iodonium, an NADH/NADPH oxidase inhibitor, attenuates angiotensin II-stimulated phosphorylation of p38MAPK, but not p42/44MAPK. Furthermore, in cells stably transfected with human catalase, angiotensin II-induced intracellular H2O2 generation is almost completely blocked, resulting in inhibition of phosphorylation of p38MAPK, but not p42/44MAPK, and a subsequent partial decrease in angiotensin II-induced hypertrophy. Specific inhibition of either the p38MAPK pathway with SB203580 (4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole) or the p42/44MAPK pathway with PD98059 (2-(2′-amino-3′-methoxyphenyl)oxanaphthalen-4-one) also partially, but significantly, attenuates angiotensin II-induced hypertrophy; however, simultaneous blockade of both pathways has an additive inhibitory effect, indicating that the hypertrophic response to angiotensin II requires parallel, independent activation of both MAPK pathways. These results provide the first evidence that p38MAPK is a Critical Component of the oxidant stress (H2O2)-sensitive signaling pathways activated by angiotensin II in vascular smooth muscle cells and indicate that it plays a crucial role in vascular hypertrophy.
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p22phox is a Critical Component of the superoxide generating nadh nadph oxidase system and regulates angiotensin ii induced hypertrophy in vascular smooth muscle cells
Journal of Biological Chemistry, 1996Co-Authors: Masuko Ushiofukai, Maziar A Zafari, Toshiki Fukui, Nobukazu Ishizaka, Kathy K GriendlingAbstract:Abstract Superoxide anion formation is vital to the microbicidal activity of phagocytes. Recently, however, there is accumulating evidence that it is also involved in cell growth in vascular smooth muscle cells (VSMCs). We have shown that the hypertrophic agent angiotensin II stimulates superoxide production by activating the membrane-bound NADH/NADPH oxidase and that inhibition of this oxidase attenuates vascular hypertrophy. However, the molecular identity of this oxidase in VSMCs is unknown. We have recently cloned the cytochrome b558 α-subunit, p22phox (one of the key electron transfer elements of the NADPH oxidase in phagocytes), from a rat VSMC cDNA library, but its role in VSMC oxidase activity remains unclarified. Here we report that the complete inhibition of p22phox mRNA expression by stable transfection of antisense p22phox cDNA into VSMCs results in a decrease in cytochrome b content, which is accompanied by a significant inhibition of angiotensin II-stimulated NADH/NADPH-dependent superoxide production, subsequent hydrogen peroxide production, and [3H]leucine incorporation. We provide the first evidence that p22phox is a Critical Component of superoxide-generating vascular NADH/NADPH oxidase and suggest a central role for this oxidase system in vascular hypertrophy.
Masuko Ushiofukai - One of the best experts on this subject based on the ideXlab platform.
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p38 mitogen activated protein kinase is a Critical Component of the redox sensitive signaling pathways activated by angiotensin ii role in vascular smooth muscle cell hypertrophy
Journal of Biological Chemistry, 1998Co-Authors: Masuko Ushiofukai, Wayne R Alexander, M Akers, Kathy K GriendlingAbstract:Abstract Angiotensin II induces an oxidant stress-dependent hypertrophy in cultured vascular smooth muscle cells. To investigate the growth-related molecular targets of H2O2, we examined the redox sensitivity of agonist-stimulated activation of the mitogen-activated protein kinase (MAPK) family. We show here that angiotensin II elicits a rapid increase in intracellular H2O2 and a rapid and robust phosphorylation of both p42/44MAPK (16-fold) and p38MAPK (15-fold). However, exogenous H2O2 activates only p38MAPK (14-fold), and diphenylene iodonium, an NADH/NADPH oxidase inhibitor, attenuates angiotensin II-stimulated phosphorylation of p38MAPK, but not p42/44MAPK. Furthermore, in cells stably transfected with human catalase, angiotensin II-induced intracellular H2O2 generation is almost completely blocked, resulting in inhibition of phosphorylation of p38MAPK, but not p42/44MAPK, and a subsequent partial decrease in angiotensin II-induced hypertrophy. Specific inhibition of either the p38MAPK pathway with SB203580 (4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole) or the p42/44MAPK pathway with PD98059 (2-(2′-amino-3′-methoxyphenyl)oxanaphthalen-4-one) also partially, but significantly, attenuates angiotensin II-induced hypertrophy; however, simultaneous blockade of both pathways has an additive inhibitory effect, indicating that the hypertrophic response to angiotensin II requires parallel, independent activation of both MAPK pathways. These results provide the first evidence that p38MAPK is a Critical Component of the oxidant stress (H2O2)-sensitive signaling pathways activated by angiotensin II in vascular smooth muscle cells and indicate that it plays a crucial role in vascular hypertrophy.
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p22phox is a Critical Component of the superoxide generating nadh nadph oxidase system and regulates angiotensin ii induced hypertrophy in vascular smooth muscle cells
Journal of Biological Chemistry, 1996Co-Authors: Masuko Ushiofukai, Maziar A Zafari, Toshiki Fukui, Nobukazu Ishizaka, Kathy K GriendlingAbstract:Abstract Superoxide anion formation is vital to the microbicidal activity of phagocytes. Recently, however, there is accumulating evidence that it is also involved in cell growth in vascular smooth muscle cells (VSMCs). We have shown that the hypertrophic agent angiotensin II stimulates superoxide production by activating the membrane-bound NADH/NADPH oxidase and that inhibition of this oxidase attenuates vascular hypertrophy. However, the molecular identity of this oxidase in VSMCs is unknown. We have recently cloned the cytochrome b558 α-subunit, p22phox (one of the key electron transfer elements of the NADPH oxidase in phagocytes), from a rat VSMC cDNA library, but its role in VSMC oxidase activity remains unclarified. Here we report that the complete inhibition of p22phox mRNA expression by stable transfection of antisense p22phox cDNA into VSMCs results in a decrease in cytochrome b content, which is accompanied by a significant inhibition of angiotensin II-stimulated NADH/NADPH-dependent superoxide production, subsequent hydrogen peroxide production, and [3H]leucine incorporation. We provide the first evidence that p22phox is a Critical Component of superoxide-generating vascular NADH/NADPH oxidase and suggest a central role for this oxidase system in vascular hypertrophy.
Wang Zhi-wei - One of the best experts on this subject based on the ideXlab platform.
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Damage Boundary Surface of Critical Components of Cubic Nonlinear Packaging System
Packaging Engineering, 2012Co-Authors: Wang Zhi-weiAbstract:Two-degree-of-freedom mathematical model of packaging system was established and analyzed.A damage evaluation method of a cubic nonlinear packaging system with Critical Component was put forward.Dynamical equations of the cubic nonlinear packaging system were solved by mathematical analysis.Based on the analysis,the damage boundary curve and damage boundary surface of Critical Component was obtained.The effect of frequency ratio,damping ratio,and pulse amplitude on the damage boundary of Critical Component was discussed.The purpose was to provide reference for material selection and structural design of transport package.
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Damage Evaluation of Hyperbolic Tangent Nonlinear Packaging System with Critical Component
Journal of Wuhan University of Technology, 2011Co-Authors: Wang Zhi-weiAbstract:The shock characteristic of the hyperbolic tangent nonlinear packaging system with Critical Component were investigated under the action of rectangular acceleration pulse.The dynamical model of the system was developed,and the numerical results of the dynamical equations were got.The damage boundary surface of Critical Component was obtained based on the results.And the effect of the pulse duration,the frequency ratio,the dmaping ratio,the pulse peak acceleration in additional to the defined system parameter on the DBS of Critical Component was discussed.It's shown that all of their effects are noticeable.The results lead to some insights into the design of cushioning packaging.
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Three-dimensional shock sprctrum of a hyperbolic tangent nonlinear packaging system with Critical Component
Journal of Vibration and Shock, 2010Co-Authors: Wang Zhi-weiAbstract:The shock characteristics of a hyperbolic tangent nonlinear packaging system with Critical Component were investigated under the action of half-sine acceleration pulse.The dynamical model of the system was developed,and the numerical results of the dynamical equations were gained.Based on the results,the three-dimensional shock response sprctrum of the Critical Component was obtained.And the effect of the pulse duration,the frequency ratio,the dmaping ratio,the pulse peak acceleration and the defined system parameters on the maximum shock response acceleration of the Critical Component was discussed.It was shown that all the effects are noticeable.
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EFFECT OF DAMPING ON THREE-DIMENSIONAL SHOCK SPECTRA OF A TANGENT PACKAGING SYSTEM WITH A Critical Component
Journal of Vibration and Shock, 2008Co-Authors: Wang Zhi-weiAbstract:Effect of damping ratio of a Critical Component and a cushioning pad on the shock characteristics of the Critical Component of a tangent packaging system are investigated under action of half-sine acceleration pulse. The dynamic model of the system is developed, and the numerical results of the dynamic equations are obtained.Then,the effect of the damping ratio on the three-dimensional shock response spectra of the Critical Component is discussed.The strong frequency ratio dependence nature of the effect is found.The peak of the shock response of the Critical Component can be decreased at low frequency ratio by increasing the damping ratio of the Critical Component,while the peak of the response of the Critical Component decreases with the rise of damping ratio of the cushioning pad at both lower and higher frequency ratio.The results lead to some insights into design of cushioning packaging.
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DAMAGE BOUNDARY SURFACE OF A TANGENT NONLINEAR PACKAGING SYSTEM WITH Critical Component
Journal of Vibration and Shock, 2008Co-Authors: Wang Zhi-weiAbstract:The shock characteristics of a tangent nonlinear packaging system with Critical Component are investigated under the action of a half-sine acceleration pulse.The dynamical model of the system is developed,and the numerical results of the dynamical equations are obtained.Then,to evaluate its damage potential,a concept of damage boundary surface is proposed,incorporating the effect of not only dimensionless Critical velocity and Critical acceleration but also frequency ratio.Based on the results,the effect of frequency ratio,pulse peak acceleration and the defined system parameter on the damage boundary of the Critical Component is discussed.It is shown that all of their effects are noticeable.The results lead to some insights into design of cushioning packaging.
Mark X Sliwkowski - One of the best experts on this subject based on the ideXlab platform.
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Growth Regulation of Human Breast and Ovarian Tumor Cells by Heregulin: Evidence for the Requirement of ErbB2 as a Critical Component in Mediating Heregulin Responsiveness
Cancer Research, 1996Co-Authors: Gail D. Lewis, Julie A. Lofgren, Amy E. Mcmurtrey, Andrew Nuijens, Brian M. Fendly, Kenneth D. Bauer, Mark X SliwkowskiAbstract:Abstract Alterations in the expression of the epidermal growth factor (EGF) receptor ErbB family are frequently encountered in a number of human cancers. Two of these receptors, ErbB3 and ErbB4, are known to bind a family of related proteins termed heregulins (HRGs) or neu differentiation factors. In biologically relevant systems, interaction of HRG with ErbB3 or ErbB4 results in the transactivation of ErbB2. In this report, we show that ErbB2 is a Critical Component in mediating HRG responsiveness in a panel of human breast and ovarian tumor cell lines. Because HRGs have been reported to elicit diverse biological effects on cultured cells, including growth stimulation, growth inhibition, and induction of differentiation, we systematically examined the effect of rHRGβ1 on tumor cell proliferation. HRG binding studies were performed with a panel of breast and ovarian tumor cell lines expressing a range of levels of ErbB2. The biological responses to HRG were also compared to EGF and to the growth-inhibitory anti-ErbB2 antibody, 4D5. In most cases, HRG stimulation of DNA synthesis correlated with positive effects on cell cycle progression and cell number and with enhancement of colony formation in soft agar. On each cell line tested, the HRG effects were distinguishable from EGF and 4D5. Our findings indicate that HRG induces cell proliferation in a number of tumor cell lines. In addition, we show that methods for measuring cell proliferation, as well as experimental conditions, are Critical for determining HRGs effect on tumor cell growth in vitro.
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growth regulation of human breast and ovarian tumor cells by heregulin evidence for the requirement of erbb2 as a Critical Component in mediating heregulin responsiveness
Cancer Research, 1996Co-Authors: Gail D. Lewis, Julie A. Lofgren, Amy E. Mcmurtrey, Andrew Nuijens, Brian M. Fendly, Kenneth D. Bauer, Mark X SliwkowskiAbstract:Alterations in the expression of the epidermal growth factor (EGF) receptor ErbB family are frequently encountered in a number of human cancers. Two of these receptors, ErbB3 and ErbB4, are known to bind a family of related proteins termed heregulins (HRGs) or neu differentiation factors. In biologically relevant systems, interaction of HRG with ErbB3 or ErbB4 results in the transactivation of ErbB2. In this report, we show that ErbB2 is a Critical Component in mediating HRG responsiveness in a panel of human breast and ovarian tumor cell lines. Because HRGs have been reported to elicit diverse biological effects on cultured cells, including growth stimulation, growth inhibition, and induction of differentiation, we systematically examined the effect of rHRG beta 1 on tumor cell proliferation. HRG binding studies were performed with a panel of breast and ovarian tumor cell lines expressing a range of levels of ErbB2. The biological responses to HRG were also compared to EGF and to the growth-inhibitory anti-ErbB2 antibody, 4D5. In most cases, HRG stimulation of DNA synthesis correlated with positive effects on cell cycle progression and cell number and with enhancement of colony formation in soft agar. On each cell line tested, the HRG effects were distinguishable from EGF and 4D5. Our findings indicate that HRG induces cell proliferation in a number of tumor cell lines. In addition, we show that methods for measuring cell proliferation, as well as experimental conditions, are Critical for determining HRGs effect on tumor cell growth in vitro.
Gail D. Lewis - One of the best experts on this subject based on the ideXlab platform.
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Growth Regulation of Human Breast and Ovarian Tumor Cells by Heregulin: Evidence for the Requirement of ErbB2 as a Critical Component in Mediating Heregulin Responsiveness
Cancer Research, 1996Co-Authors: Gail D. Lewis, Julie A. Lofgren, Amy E. Mcmurtrey, Andrew Nuijens, Brian M. Fendly, Kenneth D. Bauer, Mark X SliwkowskiAbstract:Abstract Alterations in the expression of the epidermal growth factor (EGF) receptor ErbB family are frequently encountered in a number of human cancers. Two of these receptors, ErbB3 and ErbB4, are known to bind a family of related proteins termed heregulins (HRGs) or neu differentiation factors. In biologically relevant systems, interaction of HRG with ErbB3 or ErbB4 results in the transactivation of ErbB2. In this report, we show that ErbB2 is a Critical Component in mediating HRG responsiveness in a panel of human breast and ovarian tumor cell lines. Because HRGs have been reported to elicit diverse biological effects on cultured cells, including growth stimulation, growth inhibition, and induction of differentiation, we systematically examined the effect of rHRGβ1 on tumor cell proliferation. HRG binding studies were performed with a panel of breast and ovarian tumor cell lines expressing a range of levels of ErbB2. The biological responses to HRG were also compared to EGF and to the growth-inhibitory anti-ErbB2 antibody, 4D5. In most cases, HRG stimulation of DNA synthesis correlated with positive effects on cell cycle progression and cell number and with enhancement of colony formation in soft agar. On each cell line tested, the HRG effects were distinguishable from EGF and 4D5. Our findings indicate that HRG induces cell proliferation in a number of tumor cell lines. In addition, we show that methods for measuring cell proliferation, as well as experimental conditions, are Critical for determining HRGs effect on tumor cell growth in vitro.
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growth regulation of human breast and ovarian tumor cells by heregulin evidence for the requirement of erbb2 as a Critical Component in mediating heregulin responsiveness
Cancer Research, 1996Co-Authors: Gail D. Lewis, Julie A. Lofgren, Amy E. Mcmurtrey, Andrew Nuijens, Brian M. Fendly, Kenneth D. Bauer, Mark X SliwkowskiAbstract:Alterations in the expression of the epidermal growth factor (EGF) receptor ErbB family are frequently encountered in a number of human cancers. Two of these receptors, ErbB3 and ErbB4, are known to bind a family of related proteins termed heregulins (HRGs) or neu differentiation factors. In biologically relevant systems, interaction of HRG with ErbB3 or ErbB4 results in the transactivation of ErbB2. In this report, we show that ErbB2 is a Critical Component in mediating HRG responsiveness in a panel of human breast and ovarian tumor cell lines. Because HRGs have been reported to elicit diverse biological effects on cultured cells, including growth stimulation, growth inhibition, and induction of differentiation, we systematically examined the effect of rHRG beta 1 on tumor cell proliferation. HRG binding studies were performed with a panel of breast and ovarian tumor cell lines expressing a range of levels of ErbB2. The biological responses to HRG were also compared to EGF and to the growth-inhibitory anti-ErbB2 antibody, 4D5. In most cases, HRG stimulation of DNA synthesis correlated with positive effects on cell cycle progression and cell number and with enhancement of colony formation in soft agar. On each cell line tested, the HRG effects were distinguishable from EGF and 4D5. Our findings indicate that HRG induces cell proliferation in a number of tumor cell lines. In addition, we show that methods for measuring cell proliferation, as well as experimental conditions, are Critical for determining HRGs effect on tumor cell growth in vitro.
