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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2008
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| 100 | 1 | |a Vacotto, M. | |
| 245 | 1 | 0 | |a Programmed cell death and differential JNK, p38 and ERK response in a prenatal acute hypoxic hypoxia model |
| 260 | |c 2008 | ||
| 270 | 1 | 0 | |m Fiszer de Plazas, S.; Instituto de Biología Celular y Neurociencias, Prof. E. De Robertis, Facultad de Medicina, Paraguay 2155, 1121 Buenos Aires, Argentina; email: sfiszer@fmed.uba.ar |
| 506 | |2 openaire |e Política editorial | ||
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| 520 | 3 | |a 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. |l eng | |
| 536 | |a Detalles de la financiación: Agencia Nacional de Promoción Científica y Tecnológica, PICT 38234 | ||
| 536 | |a Detalles de la financiación: Universidad de Buenos Aires, M 028 | ||
| 536 | |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas, PIP 5410 | ||
| 536 | |a Detalles de la financiación: This work was supported by grants from the Consejo Nacional de Investigaciones Científicas y Técnicas (PIP 5410), Universidad de Buenos Aires (M 028) and Agencia Nacional De Promoción Científica y Tecnológica (PICT 38234). | ||
| 593 | |a Instituto de Biología Celular y Neurociencias, Prof. E. De Robertis, Facultad de Medicina, Paraguay 2155, 1121 Buenos Aires, Argentina | ||
| 593 | |a Laboratorio de Fisiologia y Biologia Molecular, FCEyN, Universidad de Buenos Aires, 1428 Buenos Aires, Argentina | ||
| 690 | 1 | 0 | |a CHICK OPTIC LOBE |
| 690 | 1 | 0 | |a CNS DEVELOPMENT |
| 690 | 1 | 0 | |a HYPOXIA |
| 690 | 1 | 0 | |a MAPKS |
| 690 | 1 | 0 | |a PROGRAMMED CELL DEATH |
| 690 | 1 | 0 | |a 4 (4 FLUOROPHENYL) 2 (4 METHYLSULFINYLPHENYL) 5 (4 PYRIDYL)IMIDAZOLE |
| 690 | 1 | 0 | |a ANTHRA[1,9 CD]PYRAZOL 6(2H) ONE |
| 690 | 1 | 0 | |a CASPASE 3 |
| 690 | 1 | 0 | |a MITOGEN ACTIVATED PROTEIN KINASE 1 |
| 690 | 1 | 0 | |a MITOGEN ACTIVATED PROTEIN KINASE 3 |
| 690 | 1 | 0 | |a MITOGEN ACTIVATED PROTEIN KINASE P38 |
| 690 | 1 | 0 | |a STRESS ACTIVATED PROTEIN KINASE |
| 690 | 1 | 0 | |a ACUTE DISEASE |
| 690 | 1 | 0 | |a ANIMAL CELL |
| 690 | 1 | 0 | |a APOPTOSIS |
| 690 | 1 | 0 | |a ARTICLE |
| 690 | 1 | 0 | |a BRAIN DEVELOPMENT |
| 690 | 1 | 0 | |a BRAIN HYPOXIA |
| 690 | 1 | 0 | |a CELL DIFFERENTIATION |
| 690 | 1 | 0 | |a CONTROLLED STUDY |
| 690 | 1 | 0 | |a DOSE RESPONSE |
| 690 | 1 | 0 | |a DRUG INHIBITION |
| 690 | 1 | 0 | |a EMBRYO DEVELOPMENT |
| 690 | 1 | 0 | |a NICK END LABELING |
| 690 | 1 | 0 | |a NONHUMAN |
| 690 | 1 | 0 | |a OPTIC LOBE |
| 690 | 1 | 0 | |a PRENATAL PERIOD |
| 690 | 1 | 0 | |a PRIORITY JOURNAL |
| 690 | 1 | 0 | |a PROTEIN EXPRESSION |
| 690 | 1 | 0 | |a WESTERN BLOTTING |
| 690 | 1 | 0 | |a ANIMALS |
| 690 | 1 | 0 | |a APOPTOSIS |
| 690 | 1 | 0 | |a BLOTTING, WESTERN |
| 690 | 1 | 0 | |a CASPASE 3 |
| 690 | 1 | 0 | |a CHICK EMBRYO |
| 690 | 1 | 0 | |a DOSE-RESPONSE RELATIONSHIP, DRUG |
| 690 | 1 | 0 | |a ENZYME INHIBITORS |
| 690 | 1 | 0 | |a EXTRACELLULAR SIGNAL-REGULATED MAP KINASES |
| 690 | 1 | 0 | |a FETAL HYPOXIA |
| 690 | 1 | 0 | |a IN SITU NICK-END LABELING |
| 690 | 1 | 0 | |a JNK MITOGEN-ACTIVATED PROTEIN KINASES |
| 690 | 1 | 0 | |a P38 MITOGEN-ACTIVATED PROTEIN KINASES |
| 690 | 1 | 0 | |a SIGNAL TRANSDUCTION |
| 700 | 1 | |a Coso, O. | |
| 700 | 1 | |a Fiszer de Plazas, S. | |
| 773 | 0 | |d 2008 |g v. 52 |h pp. 857-863 |k n. 4-5 |p Neurochem. Int. |x 01970186 |w (AR-BaUEN)CENRE-6251 |t Neurochemistry International | |
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| 856 | 4 | 0 | |u https://hdl.handle.net/20.500.12110/paper_01970186_v52_n4-5_p857_Vacotto |y Handle |
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