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First published online June 15, 2007
Journal of Experimental Biology 210, 2267-2277 (2007)
Published by The Company of Biologists 2007
doi: 10.1242/jeb.003178

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CoCl₂ induces protective events via the p38-MAPK signalling pathway and ANP in the perfused amphibian heart

Catherine Gaitanaki, Theodora Kalpachidou, Ioanna-Katerina S. Aggeli, Panagiota Papazafiri and Isidoros Beis^*

Department of Animal and Human Physiology, School of Biology, University of Athens, Panepistimioupolis, 157 84 Athens, Greece

^* Author for correspondence (e-mail: ibeis{at}biol.uoa.gr)

Accepted 26 March 2007

Mitogen-activated protein kinases (MAPKs) constitute one of the most important intracellular signalling pathways. In particular, the p38-MAPK subfamily is known to be activated under various stressful conditions, such as mechanical or oxidative stress. Furthermore, cobalt chloride (CoCl₂) has been shown to mimic hypoxic responses in various cell lines and cause overproduction of reactive oxygen species (ROS). In the current study, we investigated the effect of CoCl₂ on p38-MAPK signalling pathway in the perfused Rana ridibunda heart. Immunoblot analysis of the phosphorylated, and thus activated, form of p38-MAPK revealed that maximum phosphorylation was attained at 500 µmol l^-1 CoCl₂. A similar profile was observed for MAPKAPK2 and Hsp27 phosphorylation (direct and indirect p38-MAPK substrates, respectively). Time course analysis of p38-MAPK phosphorylation pattern showed that the kinase reached its peak within 15 min of treatment with 500 µmol l^-1 CoCl₂. Similar results were obtained for Hsp27 phosphorylation. In the presence of the antioxidants Trolox or Lipoic acid, p38-MAPK CoCl₂-induced phosphorylation was attenuated. Analogous results were obtained for Hsp27 and MAPKAPK2. In parallel, mRNA levels of the ANP gene, a hormone whose transcriptional regulation has previously been shown to be regulated by p38-MAPK, were examined (semi-quantitative ratiometric RT-PCR). CoCl₂ treatment significantly increased ANP mRNA levels, whereas, in the presence of antioxidants, the transcript levels returned to basal values. All the above data indicate that CoCl₂ stimulates compensatory mechanisms involving the p38-MAPK signalling cascade along with ANP.

Key words: CoCl₂, hypoxia, frog heart, p38-MAPK, ANP, cardioprotection, oxidative stress, signalling

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