In this study, we found that fenvalerate affected the Ca(2+) homeostasis, inducing Ca(2+) transients via both intracellular Ca(2+) release and extracellular Ca(2+) influx. Ca(2+) influx was via store-operated channel (SOC). Therefore, the effects of fenvalerate on Ryanodine receptors (RyRs) and Inositol (1,4,5)-trisphosphate receptors (IP(3)Rs) which involved in forming Ca(2+) transient was assessed by pharmacological way.
We also demonstrated that fenvalerate affected the expression of both receptors and hindered cell proliferation as well.
In addition, we discovered that 2-APB, an antagonist of IP(3)Rs, inhibited GC-2spd (ts) cells (GC-2 cells) proliferation.
Cell cycle analysis of GC-2 cells treated with fenvalerate and 2-APB indicated that both of which showed a slight S-phase accumulation.
In conclusion, our results demonstrate that fenvalerate-induced Ca(2+) transients from both calcium release through RyRs or IP(3)Rs and calcium influx via SOC. IP(3)Rs seem to serve a predominant role in triggering Ca(2+) transients which could participate to the regulation of GC-2 cell proliferation.