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Experimental & Molecular Medicine ; : 92-97, 2008.
Article in English | WPRIM | ID: wpr-77110

ABSTRACT

Endothelins (ETs), which were originally found to be potent vasoactive transmitters, were known to be implicated in nervous system, but the mode of mechanism remains unclear. ETs (ET-1, ET-2, and ET-3) were added to HN33 (mouse hippocampal neuron chi neuroblastoma) cells. Among the three types of ET, only ET-1 increased the intracellular calcium levels in a PLC dependent manner with the induction of ERK 1/2 activation. As the result of ET-1 exposure, the survival rate of HN33 cells and the PKCalpha translocation into the plasma membrane were increased. We suggest that ET-1 participated in the neuroprotective effect involving the calcium-PKCalpha-ERK1/2 pathway.


Subject(s)
Animals , Mice , Apoptosis/drug effects , Calcium/metabolism , Cell Line , Cell Survival/drug effects , Cytosol/drug effects , Endothelin-1/pharmacology , Endothelin-2/pharmacology , Endothelin-3/pharmacology , Estrenes/pharmacology , Extracellular Signal-Regulated MAP Kinases/metabolism , Immunoblotting , Mitogen-Activated Protein Kinase 1/metabolism , Mitogen-Activated Protein Kinase 3/metabolism , Neurons/cytology , Neuroprotective Agents/pharmacology , Phosphoproteins/metabolism , Protein Kinase C-alpha/metabolism , Protein Transport/drug effects , Pyrrolidinones/pharmacology , Serum
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