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HeLa cells express cAMP-inhibitable sodium-dependent phosphate uptake
J R Raymond1, J P Middleton, V W Dennis
1Medical Service (Nephrology Section), Durham Veterans Administration Medical Center, North Carolina.
The American Journal of Physiology
|February 1, 1990
Summary
This study shows vasoactive intestinal peptide (VIP) decreases sodium-dependent phosphate uptake in HeLa cells by reducing transport maximum, not affinity. This regulation involves cyclic adenosine monophosphate (cAMP) signaling pathways.
Area of Science:
- Cellular Biology
- Molecular Physiology
- Biochemistry
Background:
- Sodium-phosphate symporter activity is crucial for phosphate homeostasis, primarily studied in renal epithelial cells.
- Receptor-mediated regulation of phosphate transport is complex and cell-type specific.
Purpose of the Study:
- To characterize sodium-dependent phosphate uptake in HeLa cells.
- To investigate the receptor-mediated regulation of phosphate uptake by vasoactive intestinal peptide (VIP) and its relation to cyclic adenosine monophosphate (cAMP) signaling.
Main Methods:
- Kinetics analysis of sodium-dependent phosphate uptake in HeLa cells.
- Treatment with VIP, forskolin, cholera toxin, and cAMP analogues (8-bromo-cAMP, dibutyryl cAMP).
- Measurement of intracellular cAMP levels and phosphate uptake rates.
Main Results:
- HeLa cells exhibit sodium-dependent phosphate uptake kinetically similar to renal cells.
- VIP stimulates intracellular cAMP levels and dose-dependently decreases phosphate uptake by reducing Vmax.
- Agents that increase cAMP, including VIP and direct cAMP analogues, inhibit phosphate uptake.
Conclusions:
- HeLa cells possess a regulated sodium-dependent phosphate transporter.
- VIP-induced inhibition of phosphate uptake is mediated through a cAMP-dependent pathway, affecting transporter maximal velocity.