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 , SerumABSTRACT
In order to investigate the expression of endothelin receptor B (ETR-B) in human malignant melanoma (MM) cells A375 and SK-mel-1 and the proliferative effects of endothelin 3 (ET3) on A375 cells, RT-PCR was applied to detect the expression of ETR-B gene in human MM cells A375 and SK-mel-1. MTT method was used to evaluate the growth enhancing effects of ET3 on A375 cell line in vitro. The results showed that ETR-B gene was expressed in both MM A375 and SK-mel-1 cells. ET3 had stronger ability to enhance the proliferation of A375 cells in vitro in a concentration-dependent manner. It was suggested that ET3/ETR-B might play an important proliferative role in MM.