Extracellular ATP causes Ca2(+)-dependent and -independent insulin secretion in RINm5F cells. Phospholipase C mediates Ca2+ mobilization but not Ca2+ influx and membrane depolarization

Li, G D; Milani, D.; Dunne, Mark J.; Pralong, William; Theler, Jean Marc; Petersen, O. H.; Wollheim, Claes B.

doi:10.1016/s0021-9258(19)67816-6

Cited by 79 publications

(2 citation statements)

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“…showed for the first time that P2Y receptors can modulate the biphasic response of insulin secretion in rat pancreas ( 49 ). This same team later reported that ADPβS, a preferential agonist of P2Y1 receptors, activates insulin secretion from perfused pancreas and isolated rat islets ( 41 , 50 , 68 ). Fischer et al.…”

Section: Extracellular Atp In Regulation Of Pancreatic ß-Cell Functionmentioning

confidence: 87%

“…Stimulation by glucose or by potassium channel inhibitors such as glibenclamide has made it possible to demonstrate the presence of ATP in the secretory granules and in particular in the insulin granules (43)(44)(45). ATP was also shown to be cosecreted with insulin during granule exocytosis and amplified glucose-induced insulin secretion by stimulating P2 receptors (46)(47)(48) and modulating the biphasic response insulin secretion in a dose-dependent manner (49,50). Furthermore, the study by Fernandez-Alvarez et al showed that P2Y receptor agonists (a, b-methylene ATP or ADPbS) amplify insulin secretion from human islets (51).…”

Section: Extracellular Atp In Regulation Of Pancreatic ß-Cell Functio...mentioning

confidence: 99%

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P2-type purinergic signaling in the regulation of pancreatic β-cell functional plasticity as a promising novel therapeutic approach for the treatment of type 2 diabetes?

2022

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Diabetes Mellitus is a metabolic disorder characterized by a chronic hyperglycemia due to an impaired insulin secretion and a decreased in peripheral insulin sensitivity. This disease is a major public health problem due to it sharp prevalence. Therefore, it is crucial to readapt therapeutic approaches for the treatment of this pathology. One of the strategies would be through P2-type purinergic receptors pathway via ATP binding. In addition to its well-known role as an intracellular energy intermediary in numerous biochemical and physiological processes, ATP is also an important extracellular signaling molecule. ATP mediates its effects by binding and activating two classes of P2 purinoreceptors: P2X receptors that are ligand-gated ion channel receptors, existing in seven isoforms (P2X 1 to 7) and P2Y receptors that are G-protein coupled receptors, existing in eight isoforms (P2Y 1/2/4/6/11/12/13/14). These receptors are ubiquitously distributed and involved in numerous physiological processes in several tissues. The concept of purinergic signaling, originally formulated by Geoffrey Burnstock (1929-2020), was also found to mediate various responses in the pancreas. Several studies have shown that P2 receptors are expressed in the endocrine pancreas, notably in β cells, where ATP could modulate their function but also their plasticity and thus play a physiological role in stimulating insulin secretion to face some metabolic demands. In this review, we provide a historical perspective and summarize current knowledge on P2-type purinergic signaling in the regulation of pancreatic β-cell functional plasticity, which would be a promising novel therapeutic approach for the treatment of type 2 diabetes.

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Section: Extracellular Atp In Regulation Of Pancreatic ß-Cell Functionmentioning

confidence: 87%

Section: Extracellular Atp In Regulation Of Pancreatic ß-Cell Functio...mentioning

confidence: 99%

P2-type purinergic signaling in the regulation of pancreatic β-cell functional plasticity as a promising novel therapeutic approach for the treatment of type 2 diabetes?

2022

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Electrophysiology of the β Cell and Mechanisms of Inhibition of Insulin Release

Dunne

Ämmälä

Straub

et al. 2001

Comprehensive Physiology

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The sections in this article are: Ion Channels in Insulin‐Secreting Cells Adenosine Triphosphate–Sensitive Potassium Channels Extracellular Control of Adenosine Triphosphate‐Sensitive Potassium Channel Function Therapeutic Manipulation by Modulators of Adenosine Triphosphate‐Sensitive Potassium Channels Architecture of the β‐cell Adenosine Triphosphate‐Sensitive Potassium Channel Calcium‐Selective Ion Channels Voltage‐Gated Sodium Channels Voltage‐Gated Potassium Channels Voltage‐Independent Potassium Channels Nonselective Cation Channels Anion‐Selective Channels Ionic Defects of β‐Cell Function Persistent Hyperinsulinemic Hypoglycemia of Infancy Altered Ionic Control of β Cells and Hypersecretion of Insulin Correlation of Gene Defects in the Adenosine Triphosphate‐Sensitive Potassium Channel with Persistent Hyperinsulinemic Hypoglycemia of Infancy Clinical Therapy for Persistent Hyperinsulinemic Hypoglycemia of Infancy Implications for Diabetes Mellitus Stimulus‐Secretion Coupling Mechanisms Other Than Depolarization Novel Methods for the Measurement of Insulin Secretion Capacitance Amperometry and Voltametry Calcium and Exocytosis Cyclic Adenosine Monophosphate and Exocytosis Effects of Phospholipases and Protein Kinases C and A Sulfonylureas and Exocytosis G Proteins and Exocytosis Other Modulators of Exocytosis Modeling Calcium‐, Cyclic, and Adenosine Monophosphate–, and Guanosine Triphosphate–Dependent Exocytosis Molecular Mechanisms of Exocytosis in the β Cell Receptor‐Mediated Inhibition of Insulin Release: Early and Late Effects Involvement of G Proteins Receptor–G Protein Interactions Inhibitory Mechanisms Adenosine Triphosphate–Sensitive Potassium Channel Activation and Membrane Repolarization Calcium Channel Inhibition Inhibition of Adenylate Cyclase Inhibition at a Distal Site G Protein–Target Interactions Adenosine Triphosphate–Sensitive Potassium Channel L‐Type Calcium Channels Adenylate Cyclase Distal Inhibitory Site Other Possible Mechanisms Inhibition of Glucose Metabolism Inhibition of Fatty Acid Metabolism Stimulation of Calcium–Adenosine Triphosphatase Activity Cyclic Guanosine Monophosphate Cytoskeleton Summary of Inhibitory Mechanisms

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Conserved transducer coupling but different effector linkage upon expression of the myeloid fMet-Leu-Phe receptor in insulin secreting cells.

Láng

Boulay

et al. 1993

The EMBO Journal

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In neutrophils fMet-Leu-Phe activates phospholipase C via a pertussis toxin sensitive G-protein and induces granule secretion. We have transfected a human cDNA sequence encoding the tMet-Leu-Phe receptor into the insulin secreting cell line RINm5F to study receptor-effector coupling with special regard to secretion. Stable overexpression resulted in membrane hyperpolarization, reduction of cAMP accumulation and inhibition of insulin secretion upon exposure of cells to fMet-Leu-Phe with EC50 values in the pmol range. As in the neutrophil, nanomolar concentrations of ligand induced membrane depolarization and activation of phospholipase C, with subsequent mobilization and influx of calcium. In permeabilized cells the inhibitory effect of fMet-Leu-Phe on secretion was partially retained indicating a direct action of the fMet-Leu-Phe receptor on exocytosis. Pertussis toxin abolished the effects of fMet-Leu-Phe. Our results suggest conserved coupling from fMet-Leu-Phe receptor to pertussis toxin sensitive transducers analogous to the mechanism in neutrophils. However, the net biological effect of receptor activation is determined by additional factors intrinsic to the host cell.

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Extracellular ATP causes Ca2(+)-dependent and -independent insulin secretion in RINm5F cells. Phospholipase C mediates Ca2+ mobilization but not Ca2+ influx and membrane depolarization

Cited by 79 publications

References 59 publications

P2-type purinergic signaling in the regulation of pancreatic β-cell functional plasticity as a promising novel therapeutic approach for the treatment of type 2 diabetes?

P2-type purinergic signaling in the regulation of pancreatic β-cell functional plasticity as a promising novel therapeutic approach for the treatment of type 2 diabetes?

Electrophysiology of the β Cell and Mechanisms of Inhibition of Insulin Release

Conserved transducer coupling but different effector linkage upon expression of the myeloid fMet-Leu-Phe receptor in insulin secreting cells.

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