Wu, Shuling; Gao, Jianping; Ohlemeyer, Carsten; Roos, Dirk; Niessen, Hans; Köttgen, Eckart; Geβner, Reinhard
Free radical biology & medicine, 2005, 2005-Dec-15, 2005-12-15, 20051215, Letnik: 39, Številka: 12Journal Article
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 1) inhibitor CV-11974 as well as by the antioxidants diphenylene iodonium (DPI) and N-acetyl- l-cysteine (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 1, resulting in effects on cardiomyocyte function such as hypertrophy.
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