Activation of AP-1 through reactive oxygen species by angiotensin II in rat cardiomyocytes
| Autor: | Jianping Gao, Carsten Ohlemeyer, Hans W.M. Niessen, Shuling Wu, Eckart Köttgen, Dirk Roos, Reinhard Gessner |
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| Přispěvatelé: | Landsteiner Laboratory |
| Jazyk: | angličtina |
| Rok vydání: | 2005 |
| Předmět: |
Time Factors
Heart Ventricles Tetrazoles HL-60 Cells medicine.disease_cause Biochemistry Antioxidants Receptor Angiotensin Type 1 chemistry.chemical_compound Onium Compounds Physiology (medical) medicine Animals Humans Myocytes Cardiac Rats Wistar Cells Cultured chemistry.chemical_classification Reactive oxygen species Angiotensin II receptor type 1 NADPH oxidase biology Dose-Response Relationship Drug Angiotensin II Biphenyl Compounds NADPH Oxidases NF-κB Molecular biology Acetylcysteine Rats Transcription Factor AP-1 chemistry cardiovascular system biology.protein Benzimidazoles Signal transduction Reactive Oxygen Species Angiotensin II Type 1 Receptor Blockers Oxidation-Reduction hormones hormone substitutes and hormone antagonists Intracellular Oxidative stress |
| Zdroj: | Free radical biology & medicine, 39(12), 1601-1610. Elsevier Inc. |
| ISSN: | 0891-5849 |
| Popis: | Cardiovascular pathogenesis induced by angiotensin II (Ang-II) is a complex process often connected to oxidative stress. In the present study we show that, 4 h after addition, Ang-II induces a four- to fivefold increase in AP-1 activity in cultured neonatal rat cardiomyocytes and that the intracellular level of reactive oxygen species (ROS) correlates with the extent of AP-1 binding activity. Ang-II stimulated ROS generation in rat cardiomyocytes in a dose- and time-dependent manner. These effects of Ang-II were suppressed by the Ang-II receptor type I (AT,) inhibitor CV-11974 as well as by the antioxidants diphenylene iodonium (DPI) and N-acetyl-(L)-eysteine (NAC), but not by AT(2) antagonist PD 122319. Furthermore, Ang-II induced a two- to threefold increase in protein synthesis and cell size during 12-24 h, which could be inhibited by CV-11974 as well as by DPI and NAC. Because the rat cardiomyocytes strongly expressed gp91(phox), this suggests that ROS generated in a gp91-containing NADPH oxidase are involved in signal transduction leading to AP-1 activation. Together, these findings indicate that Ang-II elicits the activation of the redox-sensitive AP-1 via ROS through AT,, resulting in effects on cardiomyocyte function such as hypertrophy. (c) 2005 Elsevier Inc. All rights reserved |
| Databáze: | OpenAIRE |
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