Control of Gene Expression by Catecholamines and the Renin-Angiotensin System

1. Front Matter

   Pages i-v

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2. Catecholamine Influences on Gene Expression

   1. Front Matter

      Pages 3-3

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   2. Mechanisms of transcriptional activation of cAMP-responsive element-binding protein CREB

      • Philipp Haus-Seuffert, Michael Meisterernst

      Pages 5-9

   3. Transcriptional regulation by cAMP in the heart

      • F. U. Müller, J. Neumann, W. Schmitz

      Pages 11-17

   4. Regulation of tumor growth and metastasis of human melanoma by the CREB transcription factor family

      • Didier Jean, Menashe Bar-Eli

      Pages 19-28

   5. CRE-decoy oligonucleotide-inhibition of gene expression and tumor growth

      • Yoon S. Cho-Chung, Yun Gyu Park, Maria Nesterova, Youl Nam Lee, Yee Sook Cho

      Pages 29-34

   6. Attenuation of macrophage apoptosis by the cAMP-signaling system

      • Andreas von Knethen, Bernhard Brüne

      Pages 35-43

   7. Catecholamines induce IL-10 release in patients suffering from acute myocardial infarction by transactivating its promoter in monocytic but not in T-cells

      • Ulrike Riese, Susanne Brenner, Wolf-Dietrich Döcke, Susanna Prösch, Petra Reinke, Michael Oppert et al.

      Pages 45-50

   8. Regulation of tyrosine hydroxylase gene transcription by the cAMP-signaling pathway: Involvement of multiple transcription factors

      • Jinkyu Lim, Chunying Yang, Seok Jong Hong, Kwang-Soo Kim

      Pages 51-60

   9. Norepinephrine transporter expression and function in noradrenergic cell differentiation

      • Maya Sieber-Blum, Zeguang Ren

      Pages 61-70

3. Catecholamine and Angiotensin II Influences on Gene Expression

   1. Front Matter

      Pages 71-71

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   2. Catecholamines and angiotensinogen gene expression in kidney proximal tubular cells

      • John S. D. Chan, Tian-Tian Wang, Shao-Ling Zhang, Xing Chen, Serge Carrière

      Pages 73-79

   3. cAMP increases the expression of human angiotensinogen gene through a combination of cyclic AMP responsive element binding protein and a liver specific transcription factor

      • Chittampalli S. Narayanan, Yanning Cui, Shubhra Kumar, Ashok Kumar

      Pages 81-90

   4. The role of Ca2+ mobilization and heterotrimeric G protein activation in mediating tyrosine phosphorylation signaling patterns in vascular smooth muscle cells

      • Peter P. Sayeski, M. Showkat Ali, Kenneth E. Bernstein

      Pages 91-98

   5. Functional cross-talk between the cyclic AMP and Jak/STAT signaling pathways in vascular smooth muscle cells

      • Sylvain Meloche, Stéphane Pelletier, Marc J. Servant

      Pages 99-109

   6. The inducible cAMP early repressor ICERIIγ inhibits CREB and AP-1 transcription but not AT1 receptor gene expression in vascular smooth muscle cells

      • Xiaofei Wang, T. J. Murphy

      Pages 111-119

   7. Angiotensin II-induced changes in G-protein expression and resistance of renal microvessels in young genetically hypertensive rats

      • Subhash J. Vyas, Christopher M. Blaschak, Mala R. Chinoy, Edwin K. Jackson

      Pages 121-129

   8. Angiotensin receptor II is present in dopaminergic cell line of rat substantia nigra and it is down regulated by aminochrome

      • Alexies Dagnino-Subiabre, Katerine Marcelain, Christian Arriagada, Irmgard Paris, Pablo Caviedes, Raul Caviedes et al.

      Pages 131-134

   9. Control of cardiomyocyte gene expression as drug target

      • Heinz Rupp, Martin Benkel, Bernhard Maisch

      Pages 135-142

4. Angiotensin II Influences on Gene Expression

   1. Front Matter

      Pages 143-143

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The special issue of Molecular and Cellular Biochemistry focuses on `Control of Gene Expression by Catecholamines and the Renin-Angiotensin System' in health and disease. In recent years, great progress has been made in the understanding of catecholamine and angiotensin II modulated gene expression. There is also increasing evidence that catecholamine and angiotensin II induced cellular injury not solely arises from classical pathways but also from a perturbed gene expression.
Taking into account that catecholamines and angiotensin II are vital for a balanced gene expression of many cells, the intriguing possibility arises that various disease are initiated or aggravated by such an imbalance. Catecholamine and angiotensin II influences can be in excess arising from, for example, hypercaloric food intake or psychosocial stress. During early progression of heart failure, sympathetic activity and angiotensin II influences also become increased. Due to beta-adrenergic receptor downregulation, depressed catecholamine influences are expected in the final stage of heart failure. An imbalanced influence of catecholamines and angiotensin II on gene expression leads to disordered molecular structures of the cell and an impaired cell function.
This focused issue is organized into chapters concentrating on catecholamines, angiotensin II, and the interaction between catecholamines and angiotensin II. Basic biochemical processes are covered in detail and the potential of these pathways for explaining chronic diseases associated with excess catecholamine and angiotensin II influences should become apparent. It is hoped that this focussed issue triggers novel research into the development of drugs that are targeted at diseases characterized by an imbalanced gene expression involving catecholamines and angiotensin II.

• Nucleotide
• Promoter
• biochemistry
• gene expression
• genes
• phosphorylation
• protein
• receptor
• transcription

• Internal Medicine and Cardiology, Molecular Cardiology Laboratory, Philipps University of Marburg, Marburg, Germany

  Heinz Rupp

• Internal Medical, Molecular Cardiology Laboratory, Philipps University of Marburg, Marburg, Germany

  Bernard Maisch

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