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.
Highlights
The endothelin (ET) peptides are potent peripheral vasoconstrictors and composed of 21-amino acids (Yanagisawa et al, 1988)
This study showed that ET-1-mediated effects were through PKCα-ERK1/2 pathway
These results suggest that ET-1 mediated neuroprotective effect may be due to calcium-mediated PKCα -MAPK pathways, rather than cAMP involvement
Summary
The endothelin (ET) peptides are potent peripheral vasoconstrictors and composed of 21-amino acids (Yanagisawa et al, 1988). ETs were initially believed to influence brain functions only indirectly through regulation of cerebral perfusion due to their vasoconstrictor activity. Within the CNS, ET-1 has been detected in Treatment of cultured cells with ETs. The concentrations of ETs (Sigma-Aldrich, St. Louis, MO) were determined in preliminary experiments. ETs’ effect on the calcium concentrations in HN33 cells were compared at 6 different ETs concentrations (100, 300, 900 nM and 1, 2, 3 μM). ET-1 at a concentration between 300 nM and 1 μM elicited concentration-dependent increase of intracellular calcium concentrations. According to this result, the concentration of saturation point 1 μM was chosen in this study
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