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Article: PGE generates intracellular cAMP and accelerates mucin secretion by cultured dog gallbladder epithelial cells

TitlePGE generates intracellular cAMP and accelerates mucin secretion by cultured dog gallbladder epithelial cells
Authors
Issue Date1994
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpgi.physiology.org/
Citation
American Journal Of Physiology - Gastrointestinal And Liver Physiology, 1994, v. 267 n. 6 30-6, p. G998-G1003 How to Cite?
AbstractMucin is the main secretory product of gallbladder epithelial cells. Increased gallbladder mucus secretion has been implicated in gallstone formation in humans. The mechanisms underlying control of mucin synthesis and secretion by the gallbladder are not known. This study aimed to elucidate the efficacy of a panel of secretagogues to stimulate mucin secretion and to determine the intracellular second messengers involved. Studies were carried out on normal well-differentiated epithelial cells from dog gallbladder grown in monolayer culture. Intracellular adenosine 3',5'-cyclic monophosphate (cAMP) as measured by radioimmunoassay increased in response to prostaglandin (PG) E2, PGE1, vasoactive intestinal peptide, epinephrine, and isoproterenol. The greatest effect, a 37-fold increase in cAMP level, was noted with PGE2 at 1.0 μM concentration. In contrast, three breakdown products of phosphatidylinositol (inositol triphosphate, inositol bisphosphate and inositol monophosphate) were not detected with any of the secretagogues tested. Assay of mucin secretion using tritiated N-acetyl-D- glucosamine, a mucin precursor, showed that the same secretagogues noted to increase intracellular cAMP led to an increase in mucin secretion. No correlation was noted, however, between the magnitude of the intracellular cAMP rise and the amount of mucin secreted. A membrane-permeable form of cAMP, dibutyryl cAMP, mimicked PGE2-induced mucin secretion. The results unequivocally show that secretagogue-stimulated mucin secretion in these normal gallbladder epithelial cells can proceed via a cAMP signal transduction pathway.
Persistent Identifierhttp://hdl.handle.net/10722/175709
ISSN
2015 Impact Factor: 3.297
2015 SCImago Journal Rankings: 1.936
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKuver, Ren_US
dc.contributor.authorSavard, Cen_US
dc.contributor.authorOda, Den_US
dc.contributor.authorLee, SPen_US
dc.date.accessioned2012-11-26T09:00:38Z-
dc.date.available2012-11-26T09:00:38Z-
dc.date.issued1994en_US
dc.identifier.citationAmerican Journal Of Physiology - Gastrointestinal And Liver Physiology, 1994, v. 267 n. 6 30-6, p. G998-G1003en_US
dc.identifier.issn0193-1857en_US
dc.identifier.urihttp://hdl.handle.net/10722/175709-
dc.description.abstractMucin is the main secretory product of gallbladder epithelial cells. Increased gallbladder mucus secretion has been implicated in gallstone formation in humans. The mechanisms underlying control of mucin synthesis and secretion by the gallbladder are not known. This study aimed to elucidate the efficacy of a panel of secretagogues to stimulate mucin secretion and to determine the intracellular second messengers involved. Studies were carried out on normal well-differentiated epithelial cells from dog gallbladder grown in monolayer culture. Intracellular adenosine 3',5'-cyclic monophosphate (cAMP) as measured by radioimmunoassay increased in response to prostaglandin (PG) E2, PGE1, vasoactive intestinal peptide, epinephrine, and isoproterenol. The greatest effect, a 37-fold increase in cAMP level, was noted with PGE2 at 1.0 μM concentration. In contrast, three breakdown products of phosphatidylinositol (inositol triphosphate, inositol bisphosphate and inositol monophosphate) were not detected with any of the secretagogues tested. Assay of mucin secretion using tritiated N-acetyl-D- glucosamine, a mucin precursor, showed that the same secretagogues noted to increase intracellular cAMP led to an increase in mucin secretion. No correlation was noted, however, between the magnitude of the intracellular cAMP rise and the amount of mucin secreted. A membrane-permeable form of cAMP, dibutyryl cAMP, mimicked PGE2-induced mucin secretion. The results unequivocally show that secretagogue-stimulated mucin secretion in these normal gallbladder epithelial cells can proceed via a cAMP signal transduction pathway.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpgi.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Gastrointestinal and Liver Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCyclic Amp - Biosynthesisen_US
dc.subject.meshDogsen_US
dc.subject.meshEpithelium - Metabolismen_US
dc.subject.meshGallbladder - Metabolismen_US
dc.subject.meshInositol Phosphates - Metabolismen_US
dc.subject.meshMucins - Secretionen_US
dc.subject.meshProstaglandins E - Pharmacologyen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshVasoactive Intestinal Peptide - Pharmacologyen_US
dc.titlePGE generates intracellular cAMP and accelerates mucin secretion by cultured dog gallbladder epithelial cellsen_US
dc.typeArticleen_US
dc.identifier.emailLee, SP: sumlee@hku.hken_US
dc.identifier.authorityLee, SP=rp01351en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid7810668-
dc.identifier.scopuseid_2-s2.0-0028566859en_US
dc.identifier.volume267en_US
dc.identifier.issue6 30-6en_US
dc.identifier.spageG998en_US
dc.identifier.epageG1003en_US
dc.identifier.isiWOS:A1994PY11100007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKuver, R=6701723533en_US
dc.identifier.scopusauthoridSavard, C=6701738621en_US
dc.identifier.scopusauthoridOda, D=7006186359en_US
dc.identifier.scopusauthoridLee, SP=7601417497en_US

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