Background:

β-Glycerophosphate (sodium salt hydrate) is a potent protein phosphatase inhibitor [1].

Protein phosphatase is an enzyme that removes a phosphate group from the phosphorylated amino acid residue of its target protein. Protein phosphorylation is one of the most common protein posttranslational modifications.

β-Glycerophosphate is a potent protein phosphatase inhibitor that acts as a phosphate group donor in bone cell mineralization studies [1][3]. In MC3T3-E1, ROS 17/2.8, and chick osteoblast-like cells, β-Glycerophosphate did not affect the rate of anaerobic glycolysis, but increased the medium Pi levels, suggesting that β-Glycerophosphate was hydrolyzed by bone cells. The local increase in medium Pi concentration promoted rapid mineral deposition [1]. In human bone marrow stromal cells (HBMSC) and human osteoblasts (HOB), BMP-2 resulted in mineralization of their matrix in the presence of beta-glycerophosphate and ascorbic acid [3]. β-Glycerophosphate (10 mM) also accelerated calcification of cultured vascular smooth muscle cells through an alkaline phosphatase-related mechanism [4].

参考文献:
[1].  Chung CH, Golub EE, Forbes E, et al. Mechanism of action of beta-glycerophosphate on bone cell mineralization. Calcif Tissue Int. 1992 Oct;51(4):305-11.
[2].  Fujimoto H, Mabuchi I. Isolation of cleavage furrows from eggs of regular sea urchins and identification of furrow-specific proteins. J Biochem. 1997 Sep;122(3):518-24.
[3].  Lecanda F, Avioli LV, Cheng SL. Regulation of bone matrix protein expression and induction of differentiation of human osteoblasts and human bone marrow stromal cells by bone morphogenetic protein-2. J Cell Biochem. 1997 Dec 1;67(3):386-96.
[4].  Shioi A, Nishizawa Y, Jono S, et al. Beta-glycerophosphate accelerates calcification in cultured bovine vascular smooth muscle cells. Arterioscler Thromb Vasc Biol. 1995 Nov;15(11):2003-9.