File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Induction of differentiation in v-Ha-ras-transformated MDCK cells by prostaglandin E 2 and 8-bromo-cyclic AMP is associated with a decrease in steady-state level of inositol 1,4,5-trisphosphate

TitleInduction of differentiation in v-Ha-ras-transformated MDCK cells by prostaglandin E 2 and 8-bromo-cyclic AMP is associated with a decrease in steady-state level of inositol 1,4,5-trisphosphate
Authors
Issue Date1990
Citation
Molecular And Cellular Biology, 1990, v. 10 n. 1, p. 57-67 How to Cite?
AbstractWe used Ha-ras-transformated Madin-Darby canine kidney (MDCK) cells as a model to study possible signal transduction mechanisms underlying the induction of glucagon responsiveness by the differentiation inducers prostaglandin E 2 (PGE 2) and 8-bromo-cyclic (8-Br-cAMP) AMP and the inhibition of induction by phorbol ester or a serum factor. The steady-state level of inositol 1,4,5-trisphosphate (IP 3) was higher in Ha-ras-transformed MDCK cells than in parental MDCK cells. In contrast, the steady-state level of intracellular cAMP of transformed cells was similar to that of normal cells. PGE 2 and 8-Br-cAMP increased cAMP content but decreased IP 3 levels in a concentration-dependent fashion after 5 days of treatment. We examined the time course for effects of PGE 2 and 8-Br-cAMP and found that there was a lag period of 8 to 16 h between elevation of cAMP after the addition of 8-Br-cAMP or PGE 2 and the decrease of IP 3 levels. Another lag period of 2 days existed before the induction of differentiation. Both the reduction of IP 3 levels and the induction of glucagon responsiveness were blocked by phorbol-12-myristate-13-acetate or serum, suggesting that a decrease in the IP 3 level might be causally involved in induction of differentiation in transformed MDCK cells. However, induction of differentiation was not due to changes in the expression or guanine nucleotide-binding properties of p21 protein. It is likely that cAMP has a direct regulatory effect on the phospholipid signalling pathway. We conclude that perturbation of the inositol phosphate signalling pathway may be responsible for the induction of differentiation by PGE 2 and 8-Br-cAMP in transformed MDCK cells.
Persistent Identifierhttp://hdl.handle.net/10722/167492
ISSN
2015 Impact Factor: 4.427
2015 SCImago Journal Rankings: 3.806
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWu, YYen_US
dc.contributor.authorLin, MCen_US
dc.date.accessioned2012-10-08T03:07:39Z-
dc.date.available2012-10-08T03:07:39Z-
dc.date.issued1990en_US
dc.identifier.citationMolecular And Cellular Biology, 1990, v. 10 n. 1, p. 57-67en_US
dc.identifier.issn0270-7306en_US
dc.identifier.urihttp://hdl.handle.net/10722/167492-
dc.description.abstractWe used Ha-ras-transformated Madin-Darby canine kidney (MDCK) cells as a model to study possible signal transduction mechanisms underlying the induction of glucagon responsiveness by the differentiation inducers prostaglandin E 2 (PGE 2) and 8-bromo-cyclic (8-Br-cAMP) AMP and the inhibition of induction by phorbol ester or a serum factor. The steady-state level of inositol 1,4,5-trisphosphate (IP 3) was higher in Ha-ras-transformed MDCK cells than in parental MDCK cells. In contrast, the steady-state level of intracellular cAMP of transformed cells was similar to that of normal cells. PGE 2 and 8-Br-cAMP increased cAMP content but decreased IP 3 levels in a concentration-dependent fashion after 5 days of treatment. We examined the time course for effects of PGE 2 and 8-Br-cAMP and found that there was a lag period of 8 to 16 h between elevation of cAMP after the addition of 8-Br-cAMP or PGE 2 and the decrease of IP 3 levels. Another lag period of 2 days existed before the induction of differentiation. Both the reduction of IP 3 levels and the induction of glucagon responsiveness were blocked by phorbol-12-myristate-13-acetate or serum, suggesting that a decrease in the IP 3 level might be causally involved in induction of differentiation in transformed MDCK cells. However, induction of differentiation was not due to changes in the expression or guanine nucleotide-binding properties of p21 protein. It is likely that cAMP has a direct regulatory effect on the phospholipid signalling pathway. We conclude that perturbation of the inositol phosphate signalling pathway may be responsible for the induction of differentiation by PGE 2 and 8-Br-cAMP in transformed MDCK cells.en_US
dc.languageengen_US
dc.relation.ispartofMolecular and Cellular Biologyen_US
dc.subject.mesh8-Bromo Cyclic Adenosine Monophosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Differentiation - Drug Effectsen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCell Transformation, Neoplastic - Pathologyen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshDiglycerides - Metabolismen_US
dc.subject.meshDinoprostone - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshGtp-Binding Proteins - Physiologyen_US
dc.subject.meshGenes, Rasen_US
dc.subject.meshGuanine Nucleotides - Metabolismen_US
dc.subject.meshInositol 1,4,5-Trisphosphate - Metabolismen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshOncogene Protein P21(Ras) - Physiologyen_US
dc.subject.meshPhospholipids - Metabolismen_US
dc.subject.meshTetradecanoylphorbol Acetate - Pharmacologyen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshVirulence Factors, Bordetella - Pharmacologyen_US
dc.titleInduction of differentiation in v-Ha-ras-transformated MDCK cells by prostaglandin E 2 and 8-bromo-cyclic AMP is associated with a decrease in steady-state level of inositol 1,4,5-trisphosphateen_US
dc.typeArticleen_US
dc.identifier.emailLin, MC:mcllin@hkucc.hku.hken_US
dc.identifier.authorityLin, MC=rp00746en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid2152966-
dc.identifier.scopuseid_2-s2.0-0025190508en_US
dc.identifier.volume10en_US
dc.identifier.issue1en_US
dc.identifier.spage57en_US
dc.identifier.epage67en_US
dc.identifier.isiWOS:A1990CE81900007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWu, YY=16188083500en_US
dc.identifier.scopusauthoridLin, MC=7404816359en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats