The Experts below are selected from a list of 132 Experts worldwide ranked by ideXlab platform
Francis J Miller - One of the best experts on this subject based on the ideXlab platform.
-
an oxidized extracellular Oxidation Reduction State increases nox1 expression and proliferation in vascular smooth muscle cells via epidermal growth factor receptor activation
Arteriosclerosis Thrombosis and Vascular Biology, 2010Co-Authors: Bojana Stanic, Masato Katsuyama, Francis J MillerAbstract:Objective— To examine the effect of an oxidized extracellular Oxidation-Reduction (redox) State (Eh) on the expression of NADPH oxidases in vascular cells. Methods and Results— The generation of reactive oxygen species by NADPH oxidase (Nox)-based NADPH oxidases activates redox-dependent signaling pathways and contributes to the development of “oxidative stress” in vascular disease. An oxidized plasma redox State is associated with cardiovascular disease in humans; however, the cellular mechanisms by which the extracellular redox State may cause disease are not known. Aortic segments and cultured aortic smooth muscle cells were exposed to Eh between −150 mV (reduced) and 0 mV (oxidized) by altering the concentration of cysteine and its disulfide, cystine, the predominant redox couple in plasma. A more oxidized Eh increased the expression of Nox1 and resulted in Nox1-dependent proliferation of smooth muscle cells. Oxidized Eh rapidly induced epidermal growth factor receptor phosphorylation via shedding of epidermal growth factor–like ligands from the plasma membrane and caused extracellular signal–regulated kinase 1/2–dependent phosphorylation of the transcription factors activating transcription factor-1 and cAMP-response element–binding protein. Inhibition of epidermal growth factor receptor or extracellular signal–regulated kinase 1/2 activation, or addition of small interference RNA to activating transcription factor-1, prevented the increase in Nox1 expression. Conclusion— Our results identify a novel mechanism by which extracellular oxidative stress increases expression and activity of Nox1 NADPH oxidase and contributes to vascular disease.
-
An Oxidized Extracellular Oxidation-Reduction State Increases Nox1 Expression and Proliferation in Vascular Smooth Muscle Cells Via Epidermal Growth Factor Receptor Activation
Arteriosclerosis thrombosis and vascular biology, 2010Co-Authors: Bojana Stanic, Masato Katsuyama, Francis J MillerAbstract:Objective— To examine the effect of an oxidized extracellular Oxidation-Reduction (redox) State (Eh) on the expression of NADPH oxidases in vascular cells. Methods and Results— The generation of reactive oxygen species by NADPH oxidase (Nox)-based NADPH oxidases activates redox-dependent signaling pathways and contributes to the development of “oxidative stress” in vascular disease. An oxidized plasma redox State is associated with cardiovascular disease in humans; however, the cellular mechanisms by which the extracellular redox State may cause disease are not known. Aortic segments and cultured aortic smooth muscle cells were exposed to Eh between −150 mV (reduced) and 0 mV (oxidized) by altering the concentration of cysteine and its disulfide, cystine, the predominant redox couple in plasma. A more oxidized Eh increased the expression of Nox1 and resulted in Nox1-dependent proliferation of smooth muscle cells. Oxidized Eh rapidly induced epidermal growth factor receptor phosphorylation via shedding of epidermal growth factor–like ligands from the plasma membrane and caused extracellular signal–regulated kinase 1/2–dependent phosphorylation of the transcription factors activating transcription factor-1 and cAMP-response element–binding protein. Inhibition of epidermal growth factor receptor or extracellular signal–regulated kinase 1/2 activation, or addition of small interference RNA to activating transcription factor-1, prevented the increase in Nox1 expression. Conclusion— Our results identify a novel mechanism by which extracellular oxidative stress increases expression and activity of Nox1 NADPH oxidase and contributes to vascular disease.
Bojana Stanic - One of the best experts on this subject based on the ideXlab platform.
-
an oxidized extracellular Oxidation Reduction State increases nox1 expression and proliferation in vascular smooth muscle cells via epidermal growth factor receptor activation
Arteriosclerosis Thrombosis and Vascular Biology, 2010Co-Authors: Bojana Stanic, Masato Katsuyama, Francis J MillerAbstract:Objective— To examine the effect of an oxidized extracellular Oxidation-Reduction (redox) State (Eh) on the expression of NADPH oxidases in vascular cells. Methods and Results— The generation of reactive oxygen species by NADPH oxidase (Nox)-based NADPH oxidases activates redox-dependent signaling pathways and contributes to the development of “oxidative stress” in vascular disease. An oxidized plasma redox State is associated with cardiovascular disease in humans; however, the cellular mechanisms by which the extracellular redox State may cause disease are not known. Aortic segments and cultured aortic smooth muscle cells were exposed to Eh between −150 mV (reduced) and 0 mV (oxidized) by altering the concentration of cysteine and its disulfide, cystine, the predominant redox couple in plasma. A more oxidized Eh increased the expression of Nox1 and resulted in Nox1-dependent proliferation of smooth muscle cells. Oxidized Eh rapidly induced epidermal growth factor receptor phosphorylation via shedding of epidermal growth factor–like ligands from the plasma membrane and caused extracellular signal–regulated kinase 1/2–dependent phosphorylation of the transcription factors activating transcription factor-1 and cAMP-response element–binding protein. Inhibition of epidermal growth factor receptor or extracellular signal–regulated kinase 1/2 activation, or addition of small interference RNA to activating transcription factor-1, prevented the increase in Nox1 expression. Conclusion— Our results identify a novel mechanism by which extracellular oxidative stress increases expression and activity of Nox1 NADPH oxidase and contributes to vascular disease.
-
An Oxidized Extracellular Oxidation-Reduction State Increases Nox1 Expression and Proliferation in Vascular Smooth Muscle Cells Via Epidermal Growth Factor Receptor Activation
Arteriosclerosis thrombosis and vascular biology, 2010Co-Authors: Bojana Stanic, Masato Katsuyama, Francis J MillerAbstract:Objective— To examine the effect of an oxidized extracellular Oxidation-Reduction (redox) State (Eh) on the expression of NADPH oxidases in vascular cells. Methods and Results— The generation of reactive oxygen species by NADPH oxidase (Nox)-based NADPH oxidases activates redox-dependent signaling pathways and contributes to the development of “oxidative stress” in vascular disease. An oxidized plasma redox State is associated with cardiovascular disease in humans; however, the cellular mechanisms by which the extracellular redox State may cause disease are not known. Aortic segments and cultured aortic smooth muscle cells were exposed to Eh between −150 mV (reduced) and 0 mV (oxidized) by altering the concentration of cysteine and its disulfide, cystine, the predominant redox couple in plasma. A more oxidized Eh increased the expression of Nox1 and resulted in Nox1-dependent proliferation of smooth muscle cells. Oxidized Eh rapidly induced epidermal growth factor receptor phosphorylation via shedding of epidermal growth factor–like ligands from the plasma membrane and caused extracellular signal–regulated kinase 1/2–dependent phosphorylation of the transcription factors activating transcription factor-1 and cAMP-response element–binding protein. Inhibition of epidermal growth factor receptor or extracellular signal–regulated kinase 1/2 activation, or addition of small interference RNA to activating transcription factor-1, prevented the increase in Nox1 expression. Conclusion— Our results identify a novel mechanism by which extracellular oxidative stress increases expression and activity of Nox1 NADPH oxidase and contributes to vascular disease.
T.p. Borysova - One of the best experts on this subject based on the ideXlab platform.
-
Drug management of Oxidation-Reduction State of the body in respiratory tract diseases (part 6)
CHILD`S HEALTH, 2018Co-Authors: A.e. Abaturov, A.p. Volosovets, T.p. BorysovaAbstract:В обзоре литературы приведены современные данные об антиоксидантном и противовоспалительном действии полифенолов, а также их представителей куркумина и ресвератрола при заболеваниях органов дыхания.
-
Drug management of Oxidation-Reduction State of the body in respiratory tract diseases (part 4)
CHILD`S HEALTH, 2018Co-Authors: A.e. Abaturov, A.p. Volosovets, T.p. BorysovaAbstract:The review of the literature presents modern data on antioxidant vitamins — ascorbic acid and tocopherol. Their antioxidant activity and immunomodulatory action in diseases of the respiratory system is shown.
-
Drug management of Oxidation-Reduction State of the body in respiratory tract diseases (part 3)
CHILD`S HEALTH, 2018Co-Authors: A.e. Abaturov, A.p. Volosovets, T.p. BorysovaAbstract:The review of the literature presents modern data on the group of antioxidant drugs — thiol-containing compounds. Their effect on the Oxidation-Reduction State in diseases of the respiratory system is shown.
-
Drug management of Oxidation-Reduction State of the body in respiratory tract diseases (part 2)
CHILD`S HEALTH, 2018Co-Authors: A.e. Abaturov, A.p. Volosovets, T.p. BorysovaAbstract:The review of the literature presents modern data on the activators of the transcription factor NFE2L2 and mimetics of antioxidant enzymes. Their effect on the Oxidation-Reduction State in diseases of the respiratory system is shown.
-
Influence of food products on Oxidation-Reduction State in diseases of the respiratory tract
CHILD`S HEALTH, 2017Co-Authors: A.e. Abaturov, A.p. Volosovets, T.p. BorysovaAbstract:The review of the literature presents current data on the content of antioxidants in food products. Dietary factors regulating the production of nitrogen monoxide are presented. The influence of the antioxidant diet on the probability of development and course of chronic respiratory diseases is shown.
Masato Katsuyama - One of the best experts on this subject based on the ideXlab platform.
-
an oxidized extracellular Oxidation Reduction State increases nox1 expression and proliferation in vascular smooth muscle cells via epidermal growth factor receptor activation
Arteriosclerosis Thrombosis and Vascular Biology, 2010Co-Authors: Bojana Stanic, Masato Katsuyama, Francis J MillerAbstract:Objective— To examine the effect of an oxidized extracellular Oxidation-Reduction (redox) State (Eh) on the expression of NADPH oxidases in vascular cells. Methods and Results— The generation of reactive oxygen species by NADPH oxidase (Nox)-based NADPH oxidases activates redox-dependent signaling pathways and contributes to the development of “oxidative stress” in vascular disease. An oxidized plasma redox State is associated with cardiovascular disease in humans; however, the cellular mechanisms by which the extracellular redox State may cause disease are not known. Aortic segments and cultured aortic smooth muscle cells were exposed to Eh between −150 mV (reduced) and 0 mV (oxidized) by altering the concentration of cysteine and its disulfide, cystine, the predominant redox couple in plasma. A more oxidized Eh increased the expression of Nox1 and resulted in Nox1-dependent proliferation of smooth muscle cells. Oxidized Eh rapidly induced epidermal growth factor receptor phosphorylation via shedding of epidermal growth factor–like ligands from the plasma membrane and caused extracellular signal–regulated kinase 1/2–dependent phosphorylation of the transcription factors activating transcription factor-1 and cAMP-response element–binding protein. Inhibition of epidermal growth factor receptor or extracellular signal–regulated kinase 1/2 activation, or addition of small interference RNA to activating transcription factor-1, prevented the increase in Nox1 expression. Conclusion— Our results identify a novel mechanism by which extracellular oxidative stress increases expression and activity of Nox1 NADPH oxidase and contributes to vascular disease.
-
An Oxidized Extracellular Oxidation-Reduction State Increases Nox1 Expression and Proliferation in Vascular Smooth Muscle Cells Via Epidermal Growth Factor Receptor Activation
Arteriosclerosis thrombosis and vascular biology, 2010Co-Authors: Bojana Stanic, Masato Katsuyama, Francis J MillerAbstract:Objective— To examine the effect of an oxidized extracellular Oxidation-Reduction (redox) State (Eh) on the expression of NADPH oxidases in vascular cells. Methods and Results— The generation of reactive oxygen species by NADPH oxidase (Nox)-based NADPH oxidases activates redox-dependent signaling pathways and contributes to the development of “oxidative stress” in vascular disease. An oxidized plasma redox State is associated with cardiovascular disease in humans; however, the cellular mechanisms by which the extracellular redox State may cause disease are not known. Aortic segments and cultured aortic smooth muscle cells were exposed to Eh between −150 mV (reduced) and 0 mV (oxidized) by altering the concentration of cysteine and its disulfide, cystine, the predominant redox couple in plasma. A more oxidized Eh increased the expression of Nox1 and resulted in Nox1-dependent proliferation of smooth muscle cells. Oxidized Eh rapidly induced epidermal growth factor receptor phosphorylation via shedding of epidermal growth factor–like ligands from the plasma membrane and caused extracellular signal–regulated kinase 1/2–dependent phosphorylation of the transcription factors activating transcription factor-1 and cAMP-response element–binding protein. Inhibition of epidermal growth factor receptor or extracellular signal–regulated kinase 1/2 activation, or addition of small interference RNA to activating transcription factor-1, prevented the increase in Nox1 expression. Conclusion— Our results identify a novel mechanism by which extracellular oxidative stress increases expression and activity of Nox1 NADPH oxidase and contributes to vascular disease.
A.e. Abaturov - One of the best experts on this subject based on the ideXlab platform.
-
Drug management of Oxidation-Reduction State of the body in respiratory tract diseases (part 6)
CHILD`S HEALTH, 2018Co-Authors: A.e. Abaturov, A.p. Volosovets, T.p. BorysovaAbstract:В обзоре литературы приведены современные данные об антиоксидантном и противовоспалительном действии полифенолов, а также их представителей куркумина и ресвератрола при заболеваниях органов дыхания.
-
Drug management of Oxidation-Reduction State of the body in respiratory tract diseases (part 4)
CHILD`S HEALTH, 2018Co-Authors: A.e. Abaturov, A.p. Volosovets, T.p. BorysovaAbstract:The review of the literature presents modern data on antioxidant vitamins — ascorbic acid and tocopherol. Their antioxidant activity and immunomodulatory action in diseases of the respiratory system is shown.
-
Drug management of Oxidation-Reduction State of the body in respiratory tract diseases (part 3)
CHILD`S HEALTH, 2018Co-Authors: A.e. Abaturov, A.p. Volosovets, T.p. BorysovaAbstract:The review of the literature presents modern data on the group of antioxidant drugs — thiol-containing compounds. Their effect on the Oxidation-Reduction State in diseases of the respiratory system is shown.
-
Drug management of Oxidation-Reduction State of the body in respiratory tract diseases (part 2)
CHILD`S HEALTH, 2018Co-Authors: A.e. Abaturov, A.p. Volosovets, T.p. BorysovaAbstract:The review of the literature presents modern data on the activators of the transcription factor NFE2L2 and mimetics of antioxidant enzymes. Their effect on the Oxidation-Reduction State in diseases of the respiratory system is shown.
-
Influence of food products on Oxidation-Reduction State in diseases of the respiratory tract
CHILD`S HEALTH, 2017Co-Authors: A.e. Abaturov, A.p. Volosovets, T.p. BorysovaAbstract:The review of the literature presents current data on the content of antioxidants in food products. Dietary factors regulating the production of nitrogen monoxide are presented. The influence of the antioxidant diet on the probability of development and course of chronic respiratory diseases is shown.
