• Corpus ID: 23356087

Effects of caffeine on phosphatidylinositide turnover and calcium mobilization in human neuroblastoma SK-N-SH cells.

@article{Liu2005EffectsOC,
  title={Effects of caffeine on phosphatidylinositide turnover and calcium mobilization in human neuroblastoma SK-N-SH cells.},
  author={Pei-Shan Liu and H. Tu and Lung-Sen Kao},
  journal={The Chinese journal of physiology},
  year={2005},
  volume={48 2},
  pages={
          107-13
        }
}
The effects of caffeine on receptor-controlled Ca2+ mobilization and turnover of inositol phosphates in human neuroblastoma SK-N-SH cells were studied. Caffeine inhibited both the rise in cytosolic Ca2+ concentration ([Ca2+]i) evoked by muscarinic receptor agonists and the total production of inositol phosphates in a dose-dependent manner, but to different extents. At 10 mM, caffeine inhibited agonist-evoked generation of inositol phosphates almost completely, whereas the agonist-evoked [Ca2+]i… 

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References

SHOWING 1-10 OF 41 REFERENCES

Multiple effects of caffeine on Ca2+ release and influx in human B lymphocytes.

The present report may be the first demonstration of multiple effects of caffeine on Ca2+ mobilization in single cell type and suggests the need for caution regarding use of caffeine simply as a RYR-activator to study Ca2- homeostasis in eucaryotic cells.

Inhibition of Ca2+ mobilization by caffeine in a cultured vascular smooth muscle cell line (A7r5)

Data add to the complexity of caffeine‐induced changes in [Ca2+]i and point to a possible interaction between cAMP and other second messenger systems mobilizing Ca2+i in this cell type.

Ryanodine Inhibits Caffeine‐Evoked Ca2+ Mobilization and Catecholamine Secretion from Cultured Bovine Adrenal Chromaffin Cells

Results indicate that caffeine mobilizes Ca2+ from intracellular stores, the function of which is irreversibly blocked by ryanodine, resulting in the increase in catecholamine secretion in the bovine adrenal chromaffin cell.

Caffeine-induced inhibition of inositol(1,4,5)-trisphosphate-gated calcium channels from cerebellum.

The inhibitory action of caffeine on InsP3 receptors suggests that the action of caffeine on the intracellular Ca pool must be interpreted with caution when both ryanodine receptors and InsP 3 receptors are present in the cell.

The role of caffeine-sensitive Ca2+ stores in agonist- and inositol 1,4,5-trisphosphate-induced Ca2+ release from bovine adrenal chromaffin cells.

The existence of pools 1 and 3, and the ability of agonists such as histamine to discharge pool 3 completely, supports a two-pool model in which a caffeine-sensitive CICR mechanism plays a major role in the generation of agonist-induced Ca2+ spikes in bovine chromaffin cells.

Caffeine‐Sensitive Calcium Stores in Bovine Adrenal Chromaffin Cells

The results suggest that caffeine increases [Ca2+]i by causing both Ca2+ influx and Ca2- release from intracellular pools, and support a Ca 2+ entry model in which depletion of intrace cellular Ca2+, pools controls the rate of Ca2+.

Caffeine-stimulated Ca2+ release from the intracellular stores of hepatocytes is not mediated by ryanodine receptors.

It is concluded that caffeine can specifically cause Ca2+ release from the intracellular stores of hepatocytes, but the effect is unlikely to be mediated by ryanodine receptors.

Interaction of caffeine-, IP3- and vanadate-sensitive Ca2+ pools in acinar cells of the exocrine pancreas

The data indicate the presence of at least three separate Ca2+ pools in pancreatic acinar cells: the IsCaP, CasCaP and VasCaP.