Modulation of the c-Jun N-terminal kinase activity in the embryonic heart in response to anoxia-reoxygenation: involvement of the Ca2+ and mitoKATP channels.
Details
State: Public
Version: author
Serval ID
serval:BIB_AE4324FF1432
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Modulation of the c-Jun N-terminal kinase activity in the embryonic heart in response to anoxia-reoxygenation: involvement of the Ca2+ and mitoKATP channels.
Journal
Molecular and Cellular Biochemistry
ISSN
0300-8177 (Print)
ISSN-L
0300-8177
Publication state
Published
Issued date
2008
Volume
313
Number
1-2
Pages
133-138
Language
english
Abstract
Whether the response of the fetal heart to ischemia-reperfusion is associated with activation of the c-Jun N-terminal kinase (JNK) pathway is not known. In contrast, involvement of the sarcolemmal L-type Ca2+ channel (LCC) and the mitochondrial KATP (mitoKATP) channel has been established. This work aimed at investigating the profile of JNK activity during anoxia-reoxygenation and its modulation by LCC and mitoK(ATP) channel. Hearts isolated from 4-day-old chick embryos were submitted to anoxia (30 min) and reoxygenation (60 min). Using the kinase assay method, the profile of JNK activity in the ventricle was determined every 10 min throughout anoxia-reoxygenation. Effects on JNK activity of the LCC blocker verapamil (10 nM), the mitoK(ATP) channel opener diazoxide (50 microM) and the blocker 5-hydroxydecanoate (5-HD, 500 microM), the mitochondrial Ca2+ uniporter (MCU) inhibitor Ru360 (10 microM), and the antioxidant N-(2-mercaptopropionyl) glycine (MPG, 1 mM) were determined. In untreated hearts, JNK activity was increased by 40% during anoxia and peaked fivefold relative to basal level after 30-40 min reoxygenation. This peak value was reduced by half by diazoxide and was tripled by 5-HD. Furthermore, the 5-HD-mediated stimulation of JNK activity during reoxygenation was abolished by diazoxide, verapamil or Ru360. MPG had no effect on JNK activity, whatever the conditions. None of the tested pharmacological agents altered JNK activity under basal normoxic conditions. Thus, in the embryonic heart, JNK activity exhibits a characteristic pattern during anoxia and reoxygenation and the respective open-state of LCC, MCU and mitoKATP channel can be a major determinant of JNK activity in a ROS-independent manner.
Keywords
Animals, Anoxia/enzymology, Calcium/metabolism, Calcium Channels/metabolism, Chickens, Enzyme Stability, Heart/embryology, Heart Ventricles/embryology, Heart Ventricles/enzymology, Ion Channel Gating, JNK Mitogen-Activated Protein Kinases/metabolism, Models, Biological, Potassium Channels/metabolism, Sarcolemma/metabolism
Pubmed
Web of science
Create date
21/04/2008 10:43
Last modification date
20/08/2019 16:18