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dc.contributor.authorMcEneaney, Victoria
dc.contributor.authorDooley, Ruth
dc.contributor.authorHarvey, Brian J
dc.contributor.authorThomas, Warren
dc.date.accessioned2011-04-05T15:23:40Z
dc.date.available2011-04-05T15:23:40Z
dc.date.issued2010-01
dc.identifier.citationProtein kinase D stabilizes aldosterone-induced ERK1/2 MAP kinase activation in M1 renal cortical collecting duct cells to promote cell proliferation. 2010, 118 (1-2):18-28 J. Steroid Biochem. Mol. Biol.en
dc.identifier.issn1879-1220
dc.identifier.pmid19804826
dc.identifier.doi10.1016/j.jsbmb.2009.09.014
dc.identifier.urihttp://hdl.handle.net/10147/127246
dc.description.abstractAldosterone elicits transcriptional responses in target tissues and also rapidly stimulates the activation of protein kinase signalling cascades independently of de novo protein synthesis. Here we investigated aldosterone-induced cell proliferation and extra-cellular regulated kinase 1 and 2 (ERK1/2) mitogen activated protein (MAP) kinase signalling in the M1 cortical collecting duct cell line (M1-CCD). Aldosterone promoted the proliferative growth of M1-CCD cells, an effect that was protein kinase D1 (PKD1), PKCdelta and ERK1/2-dependent. Aldosterone induced the rapid activation of ERK1/2 with peaks of activation at 2 and 10 to 30 min after hormone treatment followed by sustained activation lasting beyond 120 min. M1-CCD cells suppressed in PKD1 expression exhibited only the early, transient peaks in ERK1/2 activation without the sustained phase. Aldosterone stimulated the physical association of PKD1 with ERK1/2 within 2 min of treatment. The mineralocorticoid receptor (MR) antagonist RU28318 inhibited the early and late phases of aldosterone-induced ERK1/2 activation, and also aldosterone-induced proliferative cell growth. Aldosterone induced the sub-cellular redistribution of ERK1/2 to the nuclei at 2 min and to cytoplasmic sites, proximal to the nuclei after 30 min. This sub-cellular distribution of ERK1/2 was inhibited in cells suppressed in the expression of PKD1.
dc.language.isoenen
dc.subject.meshAcetophenones
dc.subject.meshActive Transport, Cell Nucleus
dc.subject.meshAldosterone
dc.subject.meshAldosterone Antagonists
dc.subject.meshAnimals
dc.subject.meshBenzopyrans
dc.subject.meshCell Line
dc.subject.meshCell Proliferation
dc.subject.meshCytoplasm
dc.subject.meshEnzyme Activation
dc.subject.meshEpithelial Cells
dc.subject.meshExtracellular Signal-Regulated MAP Kinases
dc.subject.meshFlavonoids
dc.subject.meshKidney Cortex
dc.subject.meshKidney Tubules, Collecting
dc.subject.meshMice
dc.subject.meshMitogen-Activated Protein Kinase 1
dc.subject.meshMitogen-Activated Protein Kinase 3
dc.subject.meshModels, Biological
dc.subject.meshPhosphorylation
dc.subject.meshProtein Binding
dc.subject.meshProtein Kinase C-delta
dc.subject.meshProtein Kinase Inhibitors
dc.subject.meshReceptor, Epidermal Growth Factor
dc.subject.meshReceptors, Mineralocorticoid
dc.subject.meshSignal Transduction
dc.subject.meshSpironolactone
dc.subject.meshTRPP Cation Channels
dc.subject.meshTyrphostins
dc.titleProtein kinase D stabilizes aldosterone-induced ERK1/2 MAP kinase activation in M1 renal cortical collecting duct cells to promote cell proliferation.en
dc.typeArticleen
dc.contributor.departmentDepartment of Molecular Medicine, Royal College of Surgeons in Ireland, Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland.en
dc.identifier.journalThe Journal of steroid biochemistry and molecular biologyen
dc.description.provinceLeinster
html.description.abstractAldosterone elicits transcriptional responses in target tissues and also rapidly stimulates the activation of protein kinase signalling cascades independently of de novo protein synthesis. Here we investigated aldosterone-induced cell proliferation and extra-cellular regulated kinase 1 and 2 (ERK1/2) mitogen activated protein (MAP) kinase signalling in the M1 cortical collecting duct cell line (M1-CCD). Aldosterone promoted the proliferative growth of M1-CCD cells, an effect that was protein kinase D1 (PKD1), PKCdelta and ERK1/2-dependent. Aldosterone induced the rapid activation of ERK1/2 with peaks of activation at 2 and 10 to 30 min after hormone treatment followed by sustained activation lasting beyond 120 min. M1-CCD cells suppressed in PKD1 expression exhibited only the early, transient peaks in ERK1/2 activation without the sustained phase. Aldosterone stimulated the physical association of PKD1 with ERK1/2 within 2 min of treatment. The mineralocorticoid receptor (MR) antagonist RU28318 inhibited the early and late phases of aldosterone-induced ERK1/2 activation, and also aldosterone-induced proliferative cell growth. Aldosterone induced the sub-cellular redistribution of ERK1/2 to the nuclei at 2 min and to cytoplasmic sites, proximal to the nuclei after 30 min. This sub-cellular distribution of ERK1/2 was inhibited in cells suppressed in the expression of PKD1.


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