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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2 Pt 1
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pubmed:dateCreated |
1996-12-5
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pubmed:abstractText |
HT29-Cl.16E and HT29-Cl.19A are two different subcloned cell lines derived from the human adenocarcinoma cell line HT-29. They are similar in their ability to grow and differentiate to polarized epithelial cells but differ in that HT29-Cl.16E is goblet cell-like with many mucin granules, whereas HT29-Cl.19A lacks mucin granules. Extracellular ATP stimulates Cl- secretion in both cell lines through luminal purinergic P20 receptors and, in HT29-Cl.16E, also mucin secretion release. To evaluate whether fusion of mucin granules is associated with an increase in Cl- conductance of the plasma membrane, the effects of two fusion inhibitors on luminal Cl- conductance were measured. Blockage of actin depolymerization with phalloidin (1 microM) inhibited purinergically stimulated but not adenosine 3',5'-cyclic monophosphate (cAMP)-stimulated luminal Cl- efflux by 50% in HT29-Cl.16E. The same treatment was without effect in HT29-Cl.19A. The fungal metabolite wortmannin, which is an inhibitor of regulated exocytosis in leukocytes, at 100 nM inhibited Cl- secretion by 70% in HT29-Cl.16E. This inhibition was not a direct effect on purinergically stimulated Cl- channels because wortmannin concentrations of up to 1 microM did not affect the secretory response in HT29-Cl.19A. The wortmannin inhibition of Cl- secretion is associated with an inhibition of granule fusion as judged by electron microscopy. The differential inhibition of Cl- secretion in the related HT-29 clones that differ with respect to the presence of mucin granules indicates that 1) the granule fusion inhibitors, phalloidin and wortmannin, have no direct inhibitory effects on purinergically and cAMP-activated Cl- channels, 2) a major portion of purinergically but not cAMP-activated Cl- channels is associated with granule fusion in HT29-Cl.16E, and 3) the signaling pathways for Cl- secretion and granule fusion are not completely identical.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Androstadienes,
http://linkedlifedata.com/resource/pubmed/chemical/Chloride Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Chlorides,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Mucins,
http://linkedlifedata.com/resource/pubmed/chemical/Phalloidine,
http://linkedlifedata.com/resource/pubmed/chemical/Polymers,
http://linkedlifedata.com/resource/pubmed/chemical/Purines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Purinergic,
http://linkedlifedata.com/resource/pubmed/chemical/wortmannin
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
271
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C612-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8770002-Actins,
pubmed-meshheading:8770002-Adenosine Triphosphate,
pubmed-meshheading:8770002-Androstadienes,
pubmed-meshheading:8770002-Cell Membrane,
pubmed-meshheading:8770002-Chloride Channels,
pubmed-meshheading:8770002-Chlorides,
pubmed-meshheading:8770002-Cytoplasmic Granules,
pubmed-meshheading:8770002-Enzyme Inhibitors,
pubmed-meshheading:8770002-Humans,
pubmed-meshheading:8770002-Intracellular Membranes,
pubmed-meshheading:8770002-Microscopy, Electron,
pubmed-meshheading:8770002-Mucins,
pubmed-meshheading:8770002-Phalloidine,
pubmed-meshheading:8770002-Polymers,
pubmed-meshheading:8770002-Purines,
pubmed-meshheading:8770002-Receptors, Purinergic,
pubmed-meshheading:8770002-Tumor Cells, Cultured
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pubmed:year |
1996
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pubmed:articleTitle |
Recruitment of purinergically stimulated Cl- channels from granule membrane to plasma membrane.
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pubmed:affiliation |
Department of Physiology, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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