Effects of extracellular calcium concentration on the glutamate release by bioactive glass (BG60S) preincubated osteoblasts

Abstract

Glutamate released by osteoblasts sharing similarities with its role in neuronal transmission is a very new scientific concept which actually changed the understanding of bone physiology. Since glutamate release is a calcium (Ca2+)-dependent process and considering that we have previously demonstrated that the dissolution of bioactive glass with 60% of silicon (BG60S) can alter osteoblast Ca2+-signaling machinery, we investigated whether BG60S induces glutamate secretion in osteoblasts and whether it requires an increase in intracellular Ca2+. Here we showed that the extracellular Ca2+ increase due to BG60S dissolution leads to an intracellular Ca2+ increase in the osteoblast, through the activation of an inositol 1,4,5-triphosphate receptor (InsP3R) and a ryanodine receptor (RyR). Additionally, we also demonstrated that glutamate released by osteoblasts can be profoundly altered by BG60S. The modulation of osteoblast glutamate released by the extracellular Ca2+ concentration opens a new window in the field of tissue engineering, since many biomaterials used for bone repair are able to increase the extracellular Ca2+ concentration due to their dissolution products.