Programmed cell death and differential JNK, p38 and ERK response in a prenatal acute hypoxic hypoxia model

We previously found that prenatal hypoxia induces a significant increase in the levels of active Caspase 3 at 60 min post-hypoxia (p-h) and in the number of TUNEL-positive pyknotic cells, which peaks at 6 h p-h. The aim of this work was to study alterations in MAPKs pathways and the effect of specif...

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Autores principales:	Vacotto, Marina, Coso, Omar Adrian
Publicado:	2008
Materias:	Chick optic lobe CNS development Hypoxia MAPKs Programmed cell death 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole anthra[1,9 cd]pyrazol 6(2h) one caspase 3 mitogen activated protein kinase 1 mitogen activated protein kinase 3 mitogen activated protein kinase p38 stress activated protein kinase acute disease animal cell apoptosis article brain development brain hypoxia cell differentiation controlled study dose response drug inhibition embryo development nick end labeling nonhuman optic lobe prenatal period priority journal protein expression Western blotting Animals Apoptosis Blotting, Western Caspase 3 Chick Embryo Dose-Response Relationship, Drug Enzyme Inhibitors Extracellular Signal-Regulated MAP Kinases Fetal Hypoxia In Situ Nick-End Labeling JNK Mitogen-Activated Protein Kinases p38 Mitogen-Activated Protein Kinases Signal Transduction
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01970186_v52_n4-5_p857_Vacotto http://hdl.handle.net/20.500.12110/paper_01970186_v52_n4-5_p857_Vacotto
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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spelling	paper:paper_01970186_v52_n4-5_p857_Vacotto2023-06-08T15:20:35Z Programmed cell death and differential JNK, p38 and ERK response in a prenatal acute hypoxic hypoxia model Vacotto, Marina Coso, Omar Adrian Chick optic lobe CNS development Hypoxia MAPKs Programmed cell death 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole anthra[1,9 cd]pyrazol 6(2h) one caspase 3 mitogen activated protein kinase 1 mitogen activated protein kinase 3 mitogen activated protein kinase p38 stress activated protein kinase acute disease animal cell apoptosis article brain development brain hypoxia cell differentiation controlled study dose response drug inhibition embryo development nick end labeling nonhuman optic lobe prenatal period priority journal protein expression Western blotting Animals Apoptosis Blotting, Western Caspase 3 Chick Embryo Dose-Response Relationship, Drug Enzyme Inhibitors Extracellular Signal-Regulated MAP Kinases Fetal Hypoxia In Situ Nick-End Labeling JNK Mitogen-Activated Protein Kinases p38 Mitogen-Activated Protein Kinases Signal Transduction We previously found that prenatal hypoxia induces a significant increase in the levels of active Caspase 3 at 60 min post-hypoxia (p-h) and in the number of TUNEL-positive pyknotic cells, which peaks at 6 h p-h. The aim of this work was to study alterations in MAPKs pathways and the effect of specific inhibitors of the JNK (SP600125) and p38 (SB203580) pathways following acute hypoxia in chick optic lobe at embryonic day (ED) 12. To this end, JNK, p38 and ERK1-2 protein kinase expression levels were determined by Western blot in both their active and inactive forms, evaluated at successive p-h times. At 10 and 30 min p-h the P-JNK/JNK ratio was 1.912 ± 0.341 and 1.920 ± 0.304, respectively. Concomitantly, at 0 min p-h the P-p38/p38 ratio was 1.657 ± 0.203. Lastly, the P-ERK/ERK ratio proving non-significant throughout. When inhibitors for JNK and p38 were used, we observed a decrease in the values of active Caspase 3 at 60 min p-h, which correlated with the control values in the parameters of TUNEL-positive cells at 6 h p-h. Analysis for P-ATF-2 demonstrated an increase in hypoxic embryos compared to control ones which was reverted in a dose-dependent manner with the use of both inhibitors. All these results indicate that at ED 12, acute hypoxia might be differentially activating JNK and p38 pathways, without affecting the ERK pathway, which in turn would be activating Caspase 3, thus leading to cell death by apoptosis. Furthermore, JNK and p38 activation precede in time the programmed cell death induced by hypoxia. © 2007 Elsevier Ltd. All rights reserved. Fil:Vacotto, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Coso, O. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2008 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01970186_v52_n4-5_p857_Vacotto http://hdl.handle.net/20.500.12110/paper_01970186_v52_n4-5_p857_Vacotto
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Chick optic lobe CNS development Hypoxia MAPKs Programmed cell death 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole anthra[1,9 cd]pyrazol 6(2h) one caspase 3 mitogen activated protein kinase 1 mitogen activated protein kinase 3 mitogen activated protein kinase p38 stress activated protein kinase acute disease animal cell apoptosis article brain development brain hypoxia cell differentiation controlled study dose response drug inhibition embryo development nick end labeling nonhuman optic lobe prenatal period priority journal protein expression Western blotting Animals Apoptosis Blotting, Western Caspase 3 Chick Embryo Dose-Response Relationship, Drug Enzyme Inhibitors Extracellular Signal-Regulated MAP Kinases Fetal Hypoxia In Situ Nick-End Labeling JNK Mitogen-Activated Protein Kinases p38 Mitogen-Activated Protein Kinases Signal Transduction
spellingShingle	Chick optic lobe CNS development Hypoxia MAPKs Programmed cell death 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole anthra[1,9 cd]pyrazol 6(2h) one caspase 3 mitogen activated protein kinase 1 mitogen activated protein kinase 3 mitogen activated protein kinase p38 stress activated protein kinase acute disease animal cell apoptosis article brain development brain hypoxia cell differentiation controlled study dose response drug inhibition embryo development nick end labeling nonhuman optic lobe prenatal period priority journal protein expression Western blotting Animals Apoptosis Blotting, Western Caspase 3 Chick Embryo Dose-Response Relationship, Drug Enzyme Inhibitors Extracellular Signal-Regulated MAP Kinases Fetal Hypoxia In Situ Nick-End Labeling JNK Mitogen-Activated Protein Kinases p38 Mitogen-Activated Protein Kinases Signal Transduction Vacotto, Marina Coso, Omar Adrian Programmed cell death and differential JNK, p38 and ERK response in a prenatal acute hypoxic hypoxia model
topic_facet	Chick optic lobe CNS development Hypoxia MAPKs Programmed cell death 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole anthra[1,9 cd]pyrazol 6(2h) one caspase 3 mitogen activated protein kinase 1 mitogen activated protein kinase 3 mitogen activated protein kinase p38 stress activated protein kinase acute disease animal cell apoptosis article brain development brain hypoxia cell differentiation controlled study dose response drug inhibition embryo development nick end labeling nonhuman optic lobe prenatal period priority journal protein expression Western blotting Animals Apoptosis Blotting, Western Caspase 3 Chick Embryo Dose-Response Relationship, Drug Enzyme Inhibitors Extracellular Signal-Regulated MAP Kinases Fetal Hypoxia In Situ Nick-End Labeling JNK Mitogen-Activated Protein Kinases p38 Mitogen-Activated Protein Kinases Signal Transduction
description	We previously found that prenatal hypoxia induces a significant increase in the levels of active Caspase 3 at 60 min post-hypoxia (p-h) and in the number of TUNEL-positive pyknotic cells, which peaks at 6 h p-h. The aim of this work was to study alterations in MAPKs pathways and the effect of specific inhibitors of the JNK (SP600125) and p38 (SB203580) pathways following acute hypoxia in chick optic lobe at embryonic day (ED) 12. To this end, JNK, p38 and ERK1-2 protein kinase expression levels were determined by Western blot in both their active and inactive forms, evaluated at successive p-h times. At 10 and 30 min p-h the P-JNK/JNK ratio was 1.912 ± 0.341 and 1.920 ± 0.304, respectively. Concomitantly, at 0 min p-h the P-p38/p38 ratio was 1.657 ± 0.203. Lastly, the P-ERK/ERK ratio proving non-significant throughout. When inhibitors for JNK and p38 were used, we observed a decrease in the values of active Caspase 3 at 60 min p-h, which correlated with the control values in the parameters of TUNEL-positive cells at 6 h p-h. Analysis for P-ATF-2 demonstrated an increase in hypoxic embryos compared to control ones which was reverted in a dose-dependent manner with the use of both inhibitors. All these results indicate that at ED 12, acute hypoxia might be differentially activating JNK and p38 pathways, without affecting the ERK pathway, which in turn would be activating Caspase 3, thus leading to cell death by apoptosis. Furthermore, JNK and p38 activation precede in time the programmed cell death induced by hypoxia. © 2007 Elsevier Ltd. All rights reserved.
author	Vacotto, Marina Coso, Omar Adrian
author_facet	Vacotto, Marina Coso, Omar Adrian
author_sort	Vacotto, Marina
title	Programmed cell death and differential JNK, p38 and ERK response in a prenatal acute hypoxic hypoxia model
title_short	Programmed cell death and differential JNK, p38 and ERK response in a prenatal acute hypoxic hypoxia model
title_full	Programmed cell death and differential JNK, p38 and ERK response in a prenatal acute hypoxic hypoxia model
title_fullStr	Programmed cell death and differential JNK, p38 and ERK response in a prenatal acute hypoxic hypoxia model
title_full_unstemmed	Programmed cell death and differential JNK, p38 and ERK response in a prenatal acute hypoxic hypoxia model
title_sort	programmed cell death and differential jnk, p38 and erk response in a prenatal acute hypoxic hypoxia model
publishDate	2008
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01970186_v52_n4-5_p857_Vacotto http://hdl.handle.net/20.500.12110/paper_01970186_v52_n4-5_p857_Vacotto
work_keys_str_mv	AT vacottomarina programmedcelldeathanddifferentialjnkp38anderkresponseinaprenatalacutehypoxichypoxiamodel AT cosoomaradrian programmedcelldeathanddifferentialjnkp38anderkresponseinaprenatalacutehypoxichypoxiamodel
_version_	1768542593808859136

Programmed cell death and differential JNK, p38 and ERK response in a prenatal acute hypoxic hypoxia model

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