Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1990-7-16
pubmed:abstractText
Ca2+, an obligatory mediator of the secretory process, acts in concert with other second messengers that further amplify or inhibit the secretory response. In this overview, we will consider the relative roles of diacylglycerol (DAG), arachidonic acid, and cyclic AMP (cAMP) in modulating Ca2(+)-dependent secretion in nonexcitable cells. DAG, a product of phospholipase C (PLC)-catalyzed breakdown of phosphoinositides, stimulates protein kinase C. Ca2+ ionophores and phorbol esters (or DAG analogues) elicit a synergistic secretory response in the exocrine pancreas and parotid gland. These findings suggest that the complete activation of secretion requires stimulation of both Ca2(+)-dependent and protein kinase C-dependent pathways. Hydrolysis of phospholipids can also lead to the liberation of arachidonic acid in secretory cells. Endogenously generated arachidonic acid inhibits polyphosphoinositide synthesis in exocrine pancreas, leading to inhibition of agonist-induced IP3 formation, Ca2(+)-mobilization and amylase secretion. By contrast, arachidonic acid and its metabolites stimulate PLC in the rabbit peritoneal neutrophil, causing Ca2(+)-mobilization and lysosomal enzyme secretion. Arachidonic acid can thus serve as a positive or negative feedback regulator of secretion induced by Ca2(+)-mobilizing agonists. Finally, in the parotid gland, stimulation of amylase secretion by norepinephrine, the physiological mediator, which stimulates both the alpha and beta adrenoceptors, requires the interaction of both Ca2+ and cAMP pathways to produce a full secretory response. These studies, taken together, indicate that phosphoinositide and cAMP-dependent pathways play coordinate roles in signal transduction, leading to the Ca2(+)-mediated secretion.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-2413839, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-2826420, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-2981403, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-3003582, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-3004128, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-3010833, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-3013206, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-3013584, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-3014651, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-3491744, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-3532145, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-3838314, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-6155077, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-6177255, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-619914, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-6207929, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-6237255, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-6271829, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-6330778, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-6411729, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-6611151, http://linkedlifedata.com/resource/pubmed/commentcorrection/2161754-6819865
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0091-6765
pubmed:author
pubmed:issnType
Print
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
35-9
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Mediators of Ca2(+)-dependent secretion.
pubmed:affiliation
Department of Pharmacology and Toxicology, Medical College of Virginia, Richmond 23298.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review