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Article: Increase in pancreatic exocrine secretion during uncoupling: Evidence for a protein kinase C-independent effect

TitleIncrease in pancreatic exocrine secretion during uncoupling: Evidence for a protein kinase C-independent effect
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date1989
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexcr
Citation
Experimental Cell Research, 1989, v. 182 n. 2, p. 349-357 How to Cite?
AbstractIt has been demonstrated that blockade of the normal communication between pancreatic acinar cells leads to an increase in amylase release. Although the physiological mechanisms that regulate the gating of gap junction channels are unknown, the involvement of protein kinase C (PKC) in the inhibition of cell coupling has been reported in various cell lines. Since the activation of PKC also stimulates amylase secretion of pancreatic acinar cells, we sought to determine whether blockers of gap junctions and activators of PKC modify basal secretion by a similar mechanism. Thus, we have studied the effects of heptanol and of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the subcellular distribution of PKC, dye coupling, and amylase release of dispersed pancreatic acini. The data show that TPA activates PKC and stimulates amylase secretion without affecting the extensive dye coupling of acinar cells. By contrast, heptanol inhibits cell-to-cell coupling and increases enzyme output without altering the subcellular distribution of PKC. Heptanol also enhances significantly the secretion evoked by TPA. These results indicate that the stimulation of amylase release caused by uncoupling of acinar cells occurs by a mechanism(s) that does not involve the activation of PKC.
Persistent Identifierhttp://hdl.handle.net/10722/132775
ISSN
2015 Impact Factor: 3.378
2015 SCImago Journal Rankings: 1.900
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChanson, Men_HK
dc.contributor.authorMeda, Pen_HK
dc.contributor.authorBruzzone, Ren_HK
dc.date.accessioned2011-03-28T09:28:54Z-
dc.date.available2011-03-28T09:28:54Z-
dc.date.issued1989en_HK
dc.identifier.citationExperimental Cell Research, 1989, v. 182 n. 2, p. 349-357en_HK
dc.identifier.issn0014-4827en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132775-
dc.description.abstractIt has been demonstrated that blockade of the normal communication between pancreatic acinar cells leads to an increase in amylase release. Although the physiological mechanisms that regulate the gating of gap junction channels are unknown, the involvement of protein kinase C (PKC) in the inhibition of cell coupling has been reported in various cell lines. Since the activation of PKC also stimulates amylase secretion of pancreatic acinar cells, we sought to determine whether blockers of gap junctions and activators of PKC modify basal secretion by a similar mechanism. Thus, we have studied the effects of heptanol and of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the subcellular distribution of PKC, dye coupling, and amylase release of dispersed pancreatic acini. The data show that TPA activates PKC and stimulates amylase secretion without affecting the extensive dye coupling of acinar cells. By contrast, heptanol inhibits cell-to-cell coupling and increases enzyme output without altering the subcellular distribution of PKC. Heptanol also enhances significantly the secretion evoked by TPA. These results indicate that the stimulation of amylase release caused by uncoupling of acinar cells occurs by a mechanism(s) that does not involve the activation of PKC.en_HK
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexcren_HK
dc.relation.ispartofExperimental Cell Researchen_HK
dc.subjectChemicals And Cas Registry Numbersen_US
dc.titleIncrease in pancreatic exocrine secretion during uncoupling: Evidence for a protein kinase C-independent effecten_HK
dc.typeArticleen_HK
dc.identifier.emailBruzzone, R: bruzzone@hkucc.hku.hken_HK
dc.identifier.authorityBruzzone, R=rp01442en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid2470604-
dc.identifier.scopuseid_2-s2.0-0024363471en_HK
dc.identifier.volume182en_HK
dc.identifier.issue2en_HK
dc.identifier.spage349en_HK
dc.identifier.epage357en_HK
dc.identifier.isiWOS:A1989AA71900006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChanson, M=7004131733en_HK
dc.identifier.scopusauthoridMeda, P=7005822187en_HK
dc.identifier.scopusauthoridBruzzone, R=7006793327en_HK

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