Regulation of parathyroid hormone release by protein kinase-C is dependent on extracellular calcium in bovine parathyroid cells.

  title={Regulation of parathyroid hormone release by protein kinase-C is dependent on extracellular calcium in bovine parathyroid cells.},
  author={Bart L Clarke and Christian Hassager and Lorraine A. Fitzpatrick},
  volume={132 3},
The purpose of this study was to evaluate regulation of PTH secretion by protein kinase-C (PKC) in adult bovine parathyroid cells. Extracellular calcium (Ca2+e) is the main physiological regulator of PTH secretion. Putative second messengers include intracellular calcium (Ca2+i), cAMP, inositol trisphosphate, and diacylglycerol (DAG). Both DAG and Ca2+i activate PKC. Certain phorbol esters mimic the effect of DAG and cause prolonged stimulation of PKC. The stimulatory phorbol esters 12-O… Expand
9 Citations
Regulation of parathyroid hormone messenger RNA levels by protein kinase A and C in bovine parathyroid cells
  • E. Moallem, J. Silver, T. Naveh-Many
  • Biology, Medicine
  • Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 1995
It is reported that protein kinases A and C regulate PTH messenger RNA levels in vitro in dispersed bovine parathyroid cells, and results suggest that both protein kinase A andC are involved in the regulation of PTH gene expression. Expand
Protein Kinase C Phosphorylation of Threonine at Position 888 in Ca2+ o -Sensing Receptor (CaR) Inhibits Coupling to Ca2+ Store Release*
This study examines the role of PKC in regulating the coupling of the CaR to Ca2+ i dynamics in fura-2-loaded human embryonic kidney cells (HEK293 cells) transiently transfected with the human parathyroid CaR and suggests that phosphorylation of theCaR is the molecular basis for the previously described effect ofPKC activation on Ca2- o -evoked changes in Ca2+. Expand
Protein Kinase C Modulates Agonist-sensitive Release of Ca2+ from Internal Stores in HEK293 Cells Overexpressing the Calcium Sensing Receptor*
Results indicate that diacylglycerol-responsive PKC isoforms differentially influence CaR agonist-induced release of Ca2+ from internal stores and the need for caution when interpreting data obtained with the latter approach. Expand
Protein Kinase C (PKC) Phosphorylation of the Ca2+ o -sensing Receptor (CaR) Modulates Functional Interaction of G Proteins with the CaR Cytoplasmic Tail*
Interestingly, truncating the receptor at 888 had an even more pronounced negative effect on CaR-elicited release of intracellular Ca2+ stores without significantly affectingCaR-mediated activation of Ca2+, suggesting that PKC phosphorylation of the CaR prevents G protein subtypes from interacting with the region of the receptor critical for releasing Ca2+. Expand
Protein Kinase C Modulates Calcium Channels in Isolated Presynaptic Nerve Terminals of Rat Hippocampus
The results suggest that the activity of presynaptic voltage‐dependent Ca2+ channels in the hippocampus is under a dynamic balance between PKC phosphorylation and protein phosphatase dephosphorylated and that both of these metabolic pathways are tonically active in the nerve terminals. Expand
Increased Receptor Stimulation Elicits Differential Calcium-sensing ReceptorT888 Dephosphorylation*
High Ca2+o-stimulated protein kinase C acts in concert with high Ca2 +o-induced phosphatase activity to generate and maintain CaR-induced Ca2-i oscillations via the dynamic phosphorylation and dephosphorylation of CaRT888. Expand
Structure-function relationship of the extracellular calcium-sensing receptor.
The extracellular calcium (Ca2+ o)-sensing receptor (CaR), originally cloned from bovine parathyroid, is a G protein-coupled receptor (GPCR) that is well conserved across species. Expand
Latent hypoparathyroidism in children with conotruncal cardiac defects.
A significant number of children with conotruncal cardiac defects have normocalcemia and a normal constitutive level of parathyroid hormone but deficient parathyro hormone secretory reserve; about 30% also have 22q11 deletions, which may put them at risk for the later development of hypocalcemic hypoparathyroidism. Expand
The pathogenesis of parathyroid gland hyperplasia in chronic renal failure.
A 58-year-old female dialysis patient was admitted to the Nephrology Department at the Hopital Necker because of severe secondary hyperparathyroidism, which led to cessation of the administration of vitamin D derivatives. Expand