Exp Mol Med.  2008 Feb;40(1):92-97. 10.3858/emm.2008.40.1.92.

Endothelin 1 protects HN33 cells from serum deprivation-induced neuronal apoptosis through Ca2+-PKCalpha-ERK pathway

Affiliations
  • 1Department of Neurology, Korea University College of Medicine, Seoul 136-705, Korea. www@medimail.co.kr

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.

Keyword

calcium; cell survival; endothelins; mitogen-activated protein kinase 1; neurons; protein kinase C

MeSH Terms

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
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