Reference : Induction of Egr-1 mRNA and protein by endothelin 1, angiotensin II and norepinephrin...
Scientific journals : Article
Human health sciences : Cardiovascular & respiratory systems
http://hdl.handle.net/10993/18336
Induction of Egr-1 mRNA and protein by endothelin 1, angiotensin II and norepinephrine in neonatal cardiac myocytes.
English
Shamim, A. [> >]
Pelzer, T. [> >]
Grohe, C. [> >]
Neyses, Ludwig mailto [University of Luxembourg > Research Office]
1999
Molecular and cellular biochemistry
195
1-2
11-7
Yes (verified by ORBilu)
International
0300-8177
NETHERLANDS
[en] Angiotensin II/physiology ; Animals ; Animals, Newborn ; Blotting, Northern ; Cells, Cultured ; DNA-Binding Proteins/biosynthesis/genetics ; Early Growth Response Protein 1 ; Endothelin-1/physiology ; Fluorescent Antibody Technique, Direct ; Gene Expression Regulation/drug effects ; Immediate-Early Proteins/biosynthesis ; Microscopy, Fluorescence ; Myocardium/chemistry/cytology/metabolism ; Norepinephrine/physiology ; Protein Biosynthesis/drug effects ; RNA, Messenger/biosynthesis/drug effects ; Rats ; Signal Transduction/drug effects ; Transcription Factors/biosynthesis/genetics
[en] The early growth response gene Egr-1 is a nuclear transcription factor known to serve as an intermediary in a broad range of signal transduction processes. Recent studies have assigned Egr-1 a new role as an amplifier of gene expression. Egr-1 mRNA is expressed in the myocardium and is rapidly induced in response to hypertrophic stimuli. However, induction of the Egr-1 protein has not yet been demonstrated in the myocardium; on the other hand, in skeletal muscle cells we have shown translational regulation of Egr-1. To further investigate the role of Egr-1 in the regulatory mechanisms of a variety of signal transduction processes we have therefore asked whether bona fide hypertrophic stimuli induce Egr-1 protein subsequently to its mRNA in neonatal rat cardiomyocytes or whether translational block occurs. In confocal laser studies the Egr-1 protein was nuclearly localized. Norepinephrine (NE, 2 microM), angiotensin II (AII, 0.1 microM), and endothelin 1 (E1, 0.1 microM) each induced the Egr-1 mRNA 6-8 fold and the Egr-1 protein 3-5 fold (n = 3, p < 0.01). Therefore, in contrast to skeletal muscle cells, these stimuli increased Egr-1 mRNA and protein levels. These results point further to the role of Egr-1 as a possible amplifier of signal transduction in the myocardium.
http://hdl.handle.net/10993/18336
http://download.springer.com/static/pdf/974/art%253A10.1023%252FA%253A1006887307568.pdf?auth66=1410942091_e058aacdab5989c6e140413a016184bd&ext=.pdf

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