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Τίτλος – Title
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Η Πρωτεϊνική Κινάση C και το Ras Ρυθμίζουν τη Γονιδιακή Έκφραση του Ντοπαμινεργικού Δείκτη TH και του Νοραδρενεργικού Δείκτη DBH PKC and Ras Differentially Regulate Gene Expression of the Dopaminergic Marker TH and Noradrenergic Marker DBH |
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Συγγραφέας – Author
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Σπύρος Θεοφιλόπουλος1,2, Εμμανουέλλα Τσιριμονάκη1, Νικόλαος Σακελλαρίδης2 και Δήμητρα Μάγκουρα1 1 Κέντρο Νευροεπιστημών, Ίδρυμα Ιατροβιολογικών Ερευνών της Ακαδημίας Αθηνών, GR-11527, Αθήνα, Ελλάς. 2Εργαστήριο Φαρμακολογίας, Τμήμα Ιατρικής, Πανεπιστήμιο Θεσσαλίας, Λάρισα, Ελλάς Spyros Theofilopoulos1,2, Emmanouella Tsirimonaki1, Nikolaos Sakellaridis2 and Dimitra Mangoura1 1Center for Neurosciences, Foundation for Biomedical Research of the Academy of Athens, GR-11527 Athens, Greece; 2Department of Pharmacology, School of Medicine, University of Thessaly, Larissa, Greece |
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Παραπομπή – Citation
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Θεοφιλόπουλος,Σ., Τσιριμονάκη,Ε., Σακελλαρίδης,Ν., Μάγκουρα,Δ. : Η Πρωτεϊνική Κινάση C και το Ras Ρυθμίζουν τη Γονιδιακή Έκφραση του Ντοπαμινεργικού Δείκτη TH και του Νοραδρενεργικού Δείκτη DBH, Επιθεώρηση Κλιν. Φαρμακολ. Φαρμακοκινητ. 25: 42-43 (2007)
Theofilopoulos,S., Tsirimonaki,E., Sakellaridis,N., Mangoura,D.: PKC and Ras Differentially Regulate Gene Expression of the Dopaminergic Marker TH and Noradrenergic Marker DBH, Epitheorese Klin. Farmakol. Farmakokinet. 25: 42-43 (2007)
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Ημερομηνία Δημοσιευσης – Publication Date
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2007 – 2007
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Γλώσσα Πλήρους Κειμένου –
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Ελληνικά – Greek |
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Λέξεις κλειδιά – Keywords
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Protein kinase C, Ras, gene expression, dopaminergic marker TH, nor-adrenergic marker DBH
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Λοιποί Όροι – Other Terms
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Άρθρο Article |
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Περίληψη – Summary
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We have successfully established for the first time in the literature cell lines from human fetal cells derived from the amniotic fluid (AF) and have documented that these cells may progress and stably express many of the same genes which define progenitor dopaminergic neurons. AF cells (AFCs) may thus provide an excellent model for studying the development of dopaminergic neurons. The dopaminergic and noradrenergic transcriptional program is highly regulated during development and in the adult, in response to activation of membrane receptor signalling cascades. Gene expression of tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine synthesis, is known to be regulated by receptors that act through protein kinase C (PKC) or Ras signaling. Therefore, we pharmacologically or genetically manipulated each signalling molecule by downregulating PKC with long term (24 h) exposure of cells to the phorbol ester TPA (12-O-tetradecanoyl-phorbol-13-acetate), by overexpressing Ras with transfection, or by downregulating activated Ras by overxepressing the GRDI domain of the neurofibromin protein, a potent Ras GAP. We found that treatment with TPA increased transcription of both TH and Nurr1 (a transcriptional ‘hub’ for the acquisition of a dopaminergic phenotype) by over 80%, whereas GRDI blocked almost all TH expression. Moreover, while Ras overexpression had no effect on these two genes, it induced the de novo expression of the noradrenergic phenotype marker DBH. Expression of VMAT2 increased with all molecular manipulations, while expression of several neuronal markers, namely Tau, b-tubulin, and syntaxin, was not affected by any condition. Interestingly, treatment of AFCs with cytochalasin, which disrupts microfilaments, caused a 50% decrease in Nurr1 transcript compared to control, a 4-fold increase in VMAT2 message, and a 40% decrease in Ptx3 message. Taken together, these studies suggest that PKC and Ras have important yet differential roles in regulating gene expression of the dopaminergic marker TH and noradrenergic marker DBH during neuronal progression.
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Αναφορές – References
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Online ISSN 1011-6575
• Elsevier’s Bibliographic Databases: Scopus, EMBASE, EMBiology, Elsevier BIOBASE
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Articles published in this Journal are Indexed or Abstracted in:
• Chemical Abstracts
• Elsevier’s Bibliographic Databases: Scopus, EMBASE, EMBiology, Elsevier BIOBASE
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Τι είναι η Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Ελληνική Έκδοση-Οδηγίες προς τους Συγγραφείς
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