ArticleThe Journal of cell biology1998
Regulation of angiotensin II-induced neuromodulation by MARCKS in brain neurons.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- MARCKS Is an Essential Regulator of Reactive Oxygen Species Production in the Monocytic Cell Type.Antioxidants (Basel, Switzerland) · 2022Article
- Role of the central renin‑angiotensin system in hypertension (Review).International journal of molecular medicine · 2021Review
- Evidence of a dysregulated vitamin D endocrine system in SARS-CoV-2 infected patient's lung cells.Scientific reports · 2021Article
- BDNF-TrkB Signaling Coupled to nPKCε and cPKCβI Modulate the Phosphorylation of the Exocytotic Protein Munc18-1 During Synaptic Activity at the Neuromuscular Junction.Frontiers in molecular neuroscience · 2018Article
- Article
- Multiscale model of dynamic neuromodulation integrating neuropeptide-induced signaling pathway activity with membrane electrophysiology.Biophysical journal · 2015Article
- Construction and analysis of the protein-protein interaction networks based on gene expression profiles of Parkinson's disease.PloS one · 2014Article
- Protein kinase Cβ is a modulator of the dopamine D2 autoreceptor-activated trafficking of the dopamine transporter.Journal of neurochemistry · 2013Article
- Angiotensin-II and MARCKS: a hydrogen peroxide- and RAC1-dependent signaling pathway in vascular endothelium.The Journal of biological chemistry · 2012Article
- Hippocampal infusions of MARCKS peptides impair memory of rats on the radial-arm maze.Brain research · 2010Article
- A current view of brain renin-angiotensin system: Is the (pro)renin receptor the missing link?Pharmacology & therapeutics · 2010Review
- Shift to an involvement of phosphatidylinositol 3-kinase in angiotensin II actions on nucleus tractus solitarii neurons of the spontaneously hypertensive rat.Circulation research · 2009Article
- Differential regulation of the renin-angiotensin system by nicotine in WKY and SHR glia.Journal of molecular neuroscience : MN · 2008Article
- Nicotine modulates the renin-angiotensin system of cultured neurons and glial cells from cardiovascular brain areas of Wistar Kyoto and spontaneously hypertensive rats.Journal of molecular neuroscience : MN · 2007Article
- Nuclear localization of SP, CGRP, and NK1R in a subpopulation of dorsal root ganglia subpopulation cells in rats.Cellular and molecular neurobiology · 2006Article
- Myristoylated alanine rich C kinase substrate (MARCKS) heterozygous mutant mice exhibit deficits in hippocampal mossy fiber-CA3 long-term potentiation.Hippocampus · 2006Article
- Molecular basis of lithium action: integration of lithium-responsive signaling and gene expression networks.Molecular psychiatry · 2003Review
- Role of phosphatidylinositol 3-kinase in angiotensin II regulation of norepinephrine neuromodulation in brain neurons of the spontaneously hypertensive rat.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Effect of reduced myristoylated alanine-rich C kinase substrate expression on hippocampal mossy fiber development and spatial learning in mutant mice: transgenic rescue and interactions with gene background.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- The Combination ofCell transplantationArticle
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4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiotensin II (Ang II) exerts chronic stimulatory actions on tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DbetaH), and the norepinephrine transporter (NET), in part, by influencing the transcription of their genes. These neuromodulatory actions of Ang II involve Ras-Raf-MAP kinase signal transduction pathways (Lu, D., H. Yang, and M.K. Raizada. 1997. J. Cell Biol. 135:1609-1617). In this study, we present evidence to demonstrate participation of another signaling pathway in these neuronal actions of Ang II. It involves activation of protein kinase C (PKC)beta subtype and phosphorylation and redistribution of myristoylated alanine-rich C kinase substrate (MARCKS) in neurites. Ang II caused a dramatic redistribution of MARCKS from neuronal varicosities to neurites. This was accompanied by a time-dependent stimulation of its phosphorylation, that was mediated by the angiotensin type 1 receptor subtype (AT1). Incubation of neurons with PKCbeta subtype specific antisense oligonucleotide (AON) significantly attenuated both redistribution and phosphorylation of MARCKS. Furthermore, depletion of MARCKS by MARCKS-AON treatment of neurons resulted in a significant decrease in Ang II-stimulated accumulation of TH and DbetaH immunoreactivities and [3H]NE uptake activity in synaptosomes. In contrast, mRNA levels of TH, DbetaH, and NET were not influenced by MARKS-AON treatment. MARCKS pep148-165, which contains PKC phosphorylation sites, inhibited Ang II stimulation of MARCKS phosphorylation and reduced the amount of TH, DbetaH, and [3H]NE uptake in neuronal synaptosomes. These observations demonstrate that phosphorylation of MARCKS by PKCbeta and its redistribution from varicosities to neurites is important in Ang II-induced synaptic accumulation of TH, DbetaH, and NE. They suggest that a coordinated stimulation of transcription of TH, DbetaH, and NET, mediated by Ras-Raf-MAP kinase followed by their transport mediated by PKCbeta-MARCKS pathway are key in persistent stimulation of Ang II's neuromodulatory actions.
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