Angiotensin peptides and inducible transcription factors.
Transcription factors are DNA-binding proteins which are able to identify specific nucleotide sequences and by binding to them may regulate the expression of genes at the level of transcription. In addition to the general transcription factors, which are basically the same for each gene transcribed by eukaryotic RNA polymerase II, more than 100 specific transcription factors have been identified so far. These specific transcription factors regulate the expression patterns of various sets of inducible genes during growth and development and enable the adjustment of cells and tissues to environmental changes. Especially the AP-1 proteins have found increasing interest, since members of these families such as c-Fos and c-Jun seem to be involved in trophic changes in peripheral organs. Many studies have also used them as marker proteins for activated neurons in the central nervous system to identify functional pathways and connections between brain nuclei. The renin-angiotensin system is implicated both in the hormonal and the central regulation of blood pressure and volume homeostasis. By binding to their specific receptors angiotensin peptides, namely angiotensin (Ang) II, have also been reported to induce the expression of a variety of inducible transcription factors (ITF) of the AP-1 and other families in peripheral organs such as kidney and blood vessels and in specific brain regions. By activating ITF, transient ligand receptor signals are transformed into long-lasting genetic changes. While the Ang II induced expression of ITF in peripheral organs seems to be associated with trophism, the physiological significance of this expression in brain nuclei with their postmitotic cells is much less clear. This contribution reviews the Ang II induced ITF expression in various tissues and discusses the possible physiological and pathophysiological consequences of the resulting changes in genetic patterns.
Blume
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Department of Pharmacology, Christian Albrechts University Kiel, Germany.
Herdegen
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Unger
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D000311:Adrenal Glands / Q000378:metabolism; D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008954:Models, Biological; D009206:Myocardium / Q000378:metabolism; D016759:Oncogene Protein p65(gag-jun) / Q000378:metabolism; D016761:Oncogene Proteins v-fos / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism; D051381:Rats; D011945:Receptors, Angiotensin / Q000378:metabolism; D012083:Renin / Q000378:metabolism; D015398:Signal Transduction; D013997:Time Factors; D014157:Transcription Factors / Q000378:metabolism*
D016759:Oncogene Protein p65(gag-jun); D016761:Oncogene Proteins v-fos; D016271:Proto-Oncogene Proteins c-myc; D011945:Receptors, Angiotensin; D014157:Transcription Factors; D000804:Angiotensin II; D012083:Renin