RESUMEN
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.
Asunto(s)
Animales , Ratones , Apoptosis/efectos de los fármacos , Calcio/metabolismo , Línea Celular , Supervivencia Celular/efectos de los fármacos , Citosol/efectos de los fármacos , Endotelina-1/farmacología , Endotelina-2/farmacología , Endotelina-3/farmacología , Estrenos/farmacología , Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Immunoblotting , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Proteína Quinasa 3 Activada por Mitógenos/metabolismo , Neuronas/citología , Fármacos Neuroprotectores/farmacología , Fosfoproteínas/metabolismo , Proteína Quinasa C-alfa/metabolismo , Transporte de Proteínas/efectos de los fármacos , Pirrolidinonas/farmacología , SueroRESUMEN
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.