Differential modulation of MAP kinases by zinc deficiency in IMR-32 cells: Role of H2O2
The influence of zinc deficiency on the modulation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK1/2), p38, and c-Jun N-terminal kinase (JNK) was studied. Using human IMR-32 cells as a model of neuronal cells, the role of oxidants on MAPKs and activator p...
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2005
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15230864_v7_n11-12_p1773_Zago http://hdl.handle.net/20.500.12110/paper_15230864_v7_n11-12_p1773_Zago |
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paper:paper_15230864_v7_n11-12_p1773_Zago2023-06-08T16:19:26Z Differential modulation of MAP kinases by zinc deficiency in IMR-32 cells: Role of H2O2 2 (2 amino 3 methoxyphenyl)chromone 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole anthra[1,9 cd]pyrazol 6(2h) one catalase DNA hydrogen peroxide mitogen activated protein kinase mitogen activated protein kinase 1 mitogen activated protein kinase 3 oxidizing agent stress activated protein kinase synaptophysin transcription factor AP 1 zinc apoptosis article binding affinity cell proliferation concentration response controlled study enzyme regulation gene expression regulation human human cell incubation time nerve cell priority journal zinc deficiency Apoptosis Catalase Cell Line Enzyme Activation Humans Hydrogen Peroxide Mitogen-Activated Protein Kinases Oxidants Phosphorylation Transcription Factor AP-1 Zinc The influence of zinc deficiency on the modulation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK1/2), p38, and c-Jun N-terminal kinase (JNK) was studied. Using human IMR-32 cells as a model of neuronal cells, the role of oxidants on MAPKs and activator protein-1 (AP-1) activation in zinc deficiency was investigated, characterizing the participation of these events in the triggering of apoptosis. Relative to controls, cells incubated in media with low zinc concentrations showed increased cell oxidants and hydrogen peroxide (H2O2) release, increased JNK and p38 activation, high nuclear AP-1-DNA binding activity, and AP-1-dependent gene expression. Catalase addition to the media prevented the increase of cellular oxidants and inhibited JNK, p38, and AP-1 activation. Low levels of ERK1/2 phosphorylation were observed in the zinc-deficient cells in association with a reduction in cell proliferation. Catalase treatment did not prevent the above events nor the increased rate of apoptosis in the zinc-deficient cells. It is first demonstrated that a decrease in cellular zinc triggers H2O2-independent, as well as H2O 2-dependent effects on MAPKs. Zinc deficiency-induced increases in cellular H2O2 can trigger the activation of JNK and p38, leading to AP-1 activation, events that are not involved in zinc deficiency-induced apoptosis. © Mary Ann Liebert, Inc. 2005 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15230864_v7_n11-12_p1773_Zago http://hdl.handle.net/20.500.12110/paper_15230864_v7_n11-12_p1773_Zago |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
2 (2 amino 3 methoxyphenyl)chromone 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole anthra[1,9 cd]pyrazol 6(2h) one catalase DNA hydrogen peroxide mitogen activated protein kinase mitogen activated protein kinase 1 mitogen activated protein kinase 3 oxidizing agent stress activated protein kinase synaptophysin transcription factor AP 1 zinc apoptosis article binding affinity cell proliferation concentration response controlled study enzyme regulation gene expression regulation human human cell incubation time nerve cell priority journal zinc deficiency Apoptosis Catalase Cell Line Enzyme Activation Humans Hydrogen Peroxide Mitogen-Activated Protein Kinases Oxidants Phosphorylation Transcription Factor AP-1 Zinc |
| spellingShingle |
2 (2 amino 3 methoxyphenyl)chromone 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole anthra[1,9 cd]pyrazol 6(2h) one catalase DNA hydrogen peroxide mitogen activated protein kinase mitogen activated protein kinase 1 mitogen activated protein kinase 3 oxidizing agent stress activated protein kinase synaptophysin transcription factor AP 1 zinc apoptosis article binding affinity cell proliferation concentration response controlled study enzyme regulation gene expression regulation human human cell incubation time nerve cell priority journal zinc deficiency Apoptosis Catalase Cell Line Enzyme Activation Humans Hydrogen Peroxide Mitogen-Activated Protein Kinases Oxidants Phosphorylation Transcription Factor AP-1 Zinc Differential modulation of MAP kinases by zinc deficiency in IMR-32 cells: Role of H2O2 |
| topic_facet |
2 (2 amino 3 methoxyphenyl)chromone 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole anthra[1,9 cd]pyrazol 6(2h) one catalase DNA hydrogen peroxide mitogen activated protein kinase mitogen activated protein kinase 1 mitogen activated protein kinase 3 oxidizing agent stress activated protein kinase synaptophysin transcription factor AP 1 zinc apoptosis article binding affinity cell proliferation concentration response controlled study enzyme regulation gene expression regulation human human cell incubation time nerve cell priority journal zinc deficiency Apoptosis Catalase Cell Line Enzyme Activation Humans Hydrogen Peroxide Mitogen-Activated Protein Kinases Oxidants Phosphorylation Transcription Factor AP-1 Zinc |
| description |
The influence of zinc deficiency on the modulation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK1/2), p38, and c-Jun N-terminal kinase (JNK) was studied. Using human IMR-32 cells as a model of neuronal cells, the role of oxidants on MAPKs and activator protein-1 (AP-1) activation in zinc deficiency was investigated, characterizing the participation of these events in the triggering of apoptosis. Relative to controls, cells incubated in media with low zinc concentrations showed increased cell oxidants and hydrogen peroxide (H2O2) release, increased JNK and p38 activation, high nuclear AP-1-DNA binding activity, and AP-1-dependent gene expression. Catalase addition to the media prevented the increase of cellular oxidants and inhibited JNK, p38, and AP-1 activation. Low levels of ERK1/2 phosphorylation were observed in the zinc-deficient cells in association with a reduction in cell proliferation. Catalase treatment did not prevent the above events nor the increased rate of apoptosis in the zinc-deficient cells. It is first demonstrated that a decrease in cellular zinc triggers H2O2-independent, as well as H2O 2-dependent effects on MAPKs. Zinc deficiency-induced increases in cellular H2O2 can trigger the activation of JNK and p38, leading to AP-1 activation, events that are not involved in zinc deficiency-induced apoptosis. © Mary Ann Liebert, Inc. |
| title |
Differential modulation of MAP kinases by zinc deficiency in IMR-32 cells: Role of H2O2 |
| title_short |
Differential modulation of MAP kinases by zinc deficiency in IMR-32 cells: Role of H2O2 |
| title_full |
Differential modulation of MAP kinases by zinc deficiency in IMR-32 cells: Role of H2O2 |
| title_fullStr |
Differential modulation of MAP kinases by zinc deficiency in IMR-32 cells: Role of H2O2 |
| title_full_unstemmed |
Differential modulation of MAP kinases by zinc deficiency in IMR-32 cells: Role of H2O2 |
| title_sort |
differential modulation of map kinases by zinc deficiency in imr-32 cells: role of h2o2 |
| publishDate |
2005 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15230864_v7_n11-12_p1773_Zago http://hdl.handle.net/20.500.12110/paper_15230864_v7_n11-12_p1773_Zago |
| _version_ |
1768541722013335552 |