Myo-inositol (MI) is an important factor in the synthesis of phosphoinositides, and, as an osmolyte, MI contributes to the regulation of cell volume. In cells of renal origin, hypertonicity causes an increase in sodium-dependent MI transporter (SMIT) mRNA levels and MI transport. However, it is unknown whether changes in osmolarity regulate transport of MI in neural or endothelial cells. In these studies, neural and endothelial cells were exposed to hyperosmotic medium for up to 48 h, and the effect on MI transport was determined. Transport of MI was maximally increased by exposing the cells to hyperosmotic medium for 24 h. Kinetic analysis of high-affinity MI transport demonstrated an increase in the apparent maximal velocity with no significant change in the apparent K(m). The hyperosmotic induction of MI transport was blocked by the addition of cycloheximide, indicating a requirement for protein synthesis, and was associated with increased levels of SMIT mRNA. In contrast to the effect of hypertonicity, exposure of neural and endothelial cells to hypotonic conditions caused a decrease in SMIT mRNA levels and MI transport in endothelial cells. These studies demonstrate that, in extrarenal cell types, changes in osmolarity also regulate SMIT activity and mRNA levels.
- bovine aortic endothelial cells
- cerebral microvessel endothelial cells
- myo-inositol metabolism
- neuroblastoma cells
- organic osmolytes
ASJC Scopus subject areas
- Cell Biology