Inorganic phosphate regulates Glvr-1 and -2 expression: Role of calcium and ERK1/2

Sodium-dependent phosphate cotransporters are key regulators of phosphate homeostasis and play a major role in mineralized tissues remodelling. However, factors influencing their expression remain under consideration. In our study, modulation of type III sodium-dependent phosphate cotransporters exp...

Full description

Saved in:
Bibliographic Details
Published inBiochemical and biophysical research communications Vol. 381; no. 2; pp. 259 - 263
Main Authors Wittrant, Y., Bourgine, A., Khoshniat, S., Alliot-Licht, B., Masson, M., Gatius, M., Rouillon, T., Weiss, P., Beck, L., Guicheux, J.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 03.04.2009
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Sodium-dependent phosphate cotransporters are key regulators of phosphate homeostasis and play a major role in mineralized tissues remodelling. However, factors influencing their expression remain under consideration. In our study, modulation of type III sodium-dependent phosphate cotransporters expression by inorganic phosphate (Pi) was investigated in the murine odontoblast-like cell line MO6-G3. Experiments were designed to determine the effects of phosphate release on dental cells during tooth decay. By real-time RT-PCR we demonstrated that Glvr-1 and -2 expressions are up-regulated by Pi. The increase in Glvr-1 and -2 expressions was correlated with ERK1/2 phosphorylation and calcium/phosphate crystals formation in cultured wells. Using calcium-free culture conditions or the specific inhibitor of ERK phosphorylation (UO126), we demonstrated that Pi effects on Glvr-1 and -2 up-regulation require the presence of calcium and involve ERK signalling pathways. This study contributes to give new insights in the control of Pi transport during carious diseases.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2009.02.034