Endothelin 1 protects HN33 cells from serum deprivation-induced neuronal apoptosis through Ca2+-PKCalpha-ERK pathway.
- Author:
Moon Ho PARK
1
;
Dae Hie LEE
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords: calcium; cell survival; endothelins; mitogen-activated protein kinase 1; neurons; protein kinase C
- MeSH: Animals; Apoptosis/*drug effects; Calcium/*metabolism; Cell Line; Cell Survival/drug effects; Cytosol/drug effects/metabolism; Endothelin-1/*pharmacology; Endothelin-2/pharmacology; Endothelin-3/pharmacology; Estrenes/pharmacology; Extracellular Signal-Regulated MAP Kinases/*metabolism; Immunoblotting; Mice; Mitogen-Activated Protein Kinase 1/metabolism; Mitogen-Activated Protein Kinase 3/metabolism; Neurons/*cytology/drug effects/*enzymology; Neuroprotective Agents/pharmacology; Phosphoproteins/metabolism; Protein Kinase C-alpha/*metabolism; Protein Transport/drug effects; Pyrrolidinones/pharmacology; Serum
- From:Experimental & Molecular Medicine 2008;40(1):92-97
- CountryRepublic of Korea
- Language:English
- 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.
