Protein kinase D stabilizes aldosterone-induced ERK1/2 MAP kinase activation in M1 renal cortical collecting duct cells to promote cell proliferation.
dc.contributor.author | McEneaney, Victoria | |
dc.contributor.author | Dooley, Ruth | |
dc.contributor.author | Harvey, Brian J | |
dc.contributor.author | Thomas, Warren | |
dc.date.accessioned | 2011-04-05T15:23:40Z | |
dc.date.available | 2011-04-05T15:23:40Z | |
dc.date.issued | 2010-01 | |
dc.identifier.citation | Protein 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.issn | 1879-1220 | |
dc.identifier.pmid | 19804826 | |
dc.identifier.doi | 10.1016/j.jsbmb.2009.09.014 | |
dc.identifier.uri | http://hdl.handle.net/10147/127246 | |
dc.description.abstract | Aldosterone 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.iso | en | en |
dc.subject.mesh | Acetophenones | |
dc.subject.mesh | Active Transport, Cell Nucleus | |
dc.subject.mesh | Aldosterone | |
dc.subject.mesh | Aldosterone Antagonists | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Benzopyrans | |
dc.subject.mesh | Cell Line | |
dc.subject.mesh | Cell Proliferation | |
dc.subject.mesh | Cytoplasm | |
dc.subject.mesh | Enzyme Activation | |
dc.subject.mesh | Epithelial Cells | |
dc.subject.mesh | Extracellular Signal-Regulated MAP Kinases | |
dc.subject.mesh | Flavonoids | |
dc.subject.mesh | Kidney Cortex | |
dc.subject.mesh | Kidney Tubules, Collecting | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Mitogen-Activated Protein Kinase 1 | |
dc.subject.mesh | Mitogen-Activated Protein Kinase 3 | |
dc.subject.mesh | Models, Biological | |
dc.subject.mesh | Phosphorylation | |
dc.subject.mesh | Protein Binding | |
dc.subject.mesh | Protein Kinase C-delta | |
dc.subject.mesh | Protein Kinase Inhibitors | |
dc.subject.mesh | Receptor, Epidermal Growth Factor | |
dc.subject.mesh | Receptors, Mineralocorticoid | |
dc.subject.mesh | Signal Transduction | |
dc.subject.mesh | Spironolactone | |
dc.subject.mesh | TRPP Cation Channels | |
dc.subject.mesh | Tyrphostins | |
dc.title | Protein kinase D stabilizes aldosterone-induced ERK1/2 MAP kinase activation in M1 renal cortical collecting duct cells to promote cell proliferation. | en |
dc.type | Article | en |
dc.contributor.department | Department of Molecular Medicine, Royal College of Surgeons in Ireland, Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland. | en |
dc.identifier.journal | The Journal of steroid biochemistry and molecular biology | en |
dc.description.province | Leinster | |
html.description.abstract | Aldosterone 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. |