Titlebook: Control of Gene Expression by Catecholamines and the Renin-Angiotensin System; Heinz Rupp,Bernard Maisch Book 2000 Springer Science+Busine

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Catecholamines induce IL-10 release in patients suffering from acute myocardial infarction by transand systemic IL-10 release in response to acute stress reactions in the absence of any systemic inflammation. . and . studies in experimental models suggest that catecholamines induce IL-10 release via a cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) dependent pathway. Here we studied pat

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Regulation of tyrosine hydroxylase gene transcription by the cAMP-signaling pathway: Involvement of cholamine neurotransmitters. TH gene expression is regulated in a cell type-specific and cAMP-dependent manner. Evidence from this laboratory and others indicates that the cAMP response element (CRE), residing at —45 to —38 bp upstream of the transcription initiation site, is essential for both basa

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cAMP increases the expression of human angiotensinogen gene through a combination of cyclic AMP resption of blood pressure. We show here that the promoter activity of reporter constructs containing human angiotensinogen promoter is increased by cAMP treatment on transient transfection in HepG2 cells. We have identified a composite cAMP responsive element, located around 840 bases upstream from the

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The inducible cAMP early repressor ICERIIγ inhibits CREB and AP-1 transcription but not AT1 receptoroth muscle cells. To test whether the transcription factor CREB is in the pathway involved in modulation of AT.-receptor gene expression, AT. receptor mRNA levels were measured after stimulation with forskolin, angiotensin II and PDGF-BB in VSMC expressing the inducible cAMP early repressor protein,

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Angiotensin II-induced changes in G-protein expression and resistance of renal microvessels in youngnomenon may occur in renal preglomerular arterioles and may involve changes in expression of GTP-binding regulatory proteins. We have examined the effects of Ang II on steady state levels of G. G. G. and G. in preglomerular arterioles from young marginally hypertensive SHR and on mean arterial press