Arachidonic Acid Regulates the Phosphoinositide Signal Transduction Pathway in Submandibular Acinar Cells

  title={Arachidonic Acid Regulates the Phosphoinositide Signal Transduction Pathway in Submandibular Acinar Cells},
  author={H. Chung and N. Fleming},
  journal={Journal of Dental Research},
  pages={1462 - 1467}
Modulation of the phosphoinositide signal transduction pathway by arachidonic acid (AA) in collagenase-dispersed rat submandibular acinar cells was investigated. The muscarinic agonist, carbachol, stimulated PIP2 hydrolysis and the generation of IP 3 to five-fold the control levels. This response was inhibited by 75% on pre-treatment of cells with AA. The AA inhibitory effect was not duplicated by a range of prostaglandins and leukotrienes and was not reversed by blockers of the cyclo-oxygenase… Expand
Regulation of phosphatidylinositol kinases by arachidonic acid in rat submandibular gland cells
It is proposed that AA regulates phosphoinositide cycle activity in submandibular gland cells by acting as a noncompetitive inhibitor of PI 4-kinase and PI(4)P 5-kinases. Expand
Muscarinic regulation of phospholipase D and its role in arachidonic acid release in rat submandibular acinar cells
The characteristics of muscarinic cholinergic-induced phospholipase D (PLD) activation, and the involvement of the enzyme in the release of arachidonic acid were examined in rat submandibular acinarExpand
Arachidonic Acid Stimulates Intracellular Calcium Mobilization and Regulates Protein Synthesis, ATP Levels, and Mucin Secretion in Submandibular Gland Cells
It is concluded that arachidonic acid acts as a regulator of central synthetic/secretory processes in mucous acinar cells of rat submandibular gland and suggested that at least some of its effects may be secondary to its calcium-mobilizing action. Expand
Arachidonic Acid Inhibition of Muscarinic Receptor-Mediated Nitric Oxide Production Occurs at the Level of Calcium Mobilization in Chinese Hamster Ovary Cells
Investigation of the effects of exogenous AA on signal transduction of M1 muscarinic acetylcholine receptors in a model system of stably transfected Chinese hamster ovary cells supports the concept that AA concentration-dependently inhibits receptor-mediated NO production at the level of calcium mobilization. Expand
Phosphorylation of protein kinase B, the key enzyme in insulin-signaling cascade, is enhanced in linoleic and arachidonic acid-treated HT29 and HepG2 cells.
It is demonstrated that plasma membrane lipid bilayer enrichment with LNA or ARA treatment enhances insulin action by AKT activation, and consequently on the insulin-signaling pathway and specifically AKT phosphorylation. Expand


Arachidonic acid stimulates phosphoinositide hydrolysis and human placental lactogen release in an enriched fraction of placental cells.
The results suggest that the stimulation of hPL release by arachidonic acid may be mediated, at least in part, by the activation of phospholipase C. Expand
Inhibition of inositol phospholipids metabolism and calcium mobilization by cyclic AMP-increasing agents and phorbol ester in neutrophils.
It is suggested that cAMP inhibits the fMLP-induced Ca2+ influx, while TPA stimulates Ca2- removal from cytosol. Expand
The effects of fatty acids on phosphoinositide synthesis and myo-inositol accumulation in exocrine pancreas.
Observations suggest that in exocrine pancreas, endogenous arachidonic acid serves as a negative feedback regulator of phosphoinositide turnover, and the degree of unsaturation of the fatty acid, rather than chain length, is important for inhibition of phosphate-based synthesis. Expand
Inhibitory effects of arachidonic acid on muscarinic current response in single pancreatic acinar cells of rats.
  • Y. Maruyama
  • Medicine, Chemistry
  • The Journal of physiology
  • 1990
The results suggest that an increase in [Ca2+]i, induced by IP3 injection, activates PLA2, and that this resultant release of AA in turn inhibits IP3‐dependent Ca2+ mobilization. Expand
Analysis of the regulation of phosphatidylinositol-4,5-bisphosphate synthesis by arachidonic acid in exocrine pancreas.
In pancreatic acinar cells prelabeled with either 32Pi or myo-[3H]inositol, arachidonic acid (10-50 microM) rapidly decreased the steady-state levels of [32P]phosphatidylinositol 4',5'-bisphosphateExpand
Muscarinic, alpha 1-adrenergic and peptidergic agonists stimulate phosphoinositide hydrolysis and regulate mucin secretion in rat submandibular gland cells.
The study indicates a role for Ca2+-mobilizing agonists in controlling submandibular mucin secretion and provides evidence that receptor-linked phosphoinositide hydrolysis is an early stage in their stimulus-secretion coupling mechanism. Expand
Lipoxygenase metabolites of arachidonic acid modulate hematopoiesis.
Certain LPO products may be important mediators of both CSF- and PMA-induced myelopoiesis, and of BPA/EPO-induced erythropoies isis. Expand
adivation of phospholipase Az via GTP- binding proteins: arachidonic acid and its metabolites as second messengers
This review describes another effector system that is linked to a G protein - phoepholipase A2, which generates second messengers capable of eliciting the biological responses characteristic of that cell. Expand
Arachidonic acid‐induced mobilization of calcium in human neutrophils: evidence for a multicomponent mechanism of action
The data presented indicate that the mechanism of mobilization of calcium by arachidonic acid in human neutrophils is complex and involves specific activation pathways employed, in part at least, by other neutrophil agonists. Expand
Arachidonic acid and related methyl ester mediate protein kinase C activation in intact platelets through the arachidonate metabolism pathways.
Arachidonic acid and its methyl ester activate protein kinase C in platelets mainly through action of their metabolites and eicosanoid synthesis, which may account for the tumor-promoting activity of unsaturated fatty acids and related methyl esters. Expand