Arginine‐Modulated Receptor‐Activated Calcium Influx via a NO/Cyclic GMP Pathway in Human SK‐N‐SH Neuroblastoma Cells

Abstract

Abstract:The effects of arginine on calcium mobilization in human SK-N-SH neuroblastoma cells were examined. It was found that arginine potentiated an increase in carbachol-induced Ca 2~from the external Ca2~influx as opposed to an internal Ca2~release from intracellular pools. The potentiation effect of arginine on carbacholinduced calcium mobilization was mimicked by either 8-bromo cyclic GMP or sodium nitroprusside. In addition, it was found that arginine induced NO production and an increase in cyclic GMP. Moreover, arginine-induced potentiation, NO production, and cyclic GMP increases were all suppressed after the preincubation of cells with N-methyl-L-arginine or N-nitro-L-arginine, nitric oxide synthase inhibitor. It is suggested that the NO production and subsequent cyclic GMP elevation induced by arginine are responsible for the potentiation of carbacholinduced Ca2~increase. Our results show the existence of a NO/cyclic GMP pathway and an interconnection of NO and Ca2signaling pathways in human SK-N-SH neuroblastoma cells. We also observed that NO, which is produced by endothelial CPAE cells, has a modulating effect on cyclic GMP elevation in human SK-N-SH neuroblastoma cells. The intercellular communication role of NO and its cell-diffusing character may also affect the regulation of nonneuronal cells in their interactions with neuronal cells.

Arginine promotes myogenic differentiation and myotube formation through the elevation of cytoplasmic calcium concentration

“…The absence of RyR1 or Cav1.1 will lead to partially severe histological changes in limb skeletal muscle both at the beginning and, more so, the end of secondary myogenesis ( Filipova et al., 2018 ). Although cytoplasmic Ca 2+ appears to be coupled with a variety of functions performed by arginine ( Liu and Shaw, 1997 ; Weinhaus et al., 1997 ), its role in arginine-induced myogenic differentiation remains unknown.…”