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Activation of AP-1 through reactive oxygen species by angiotensin II in rat cardiomyocytes.
Free Radic Biol Med. 2005 Dec 15; 39(12):1601-10.FR

Abstract

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 (AT1) inhibitor CV-11974 as well as by the antioxidants diphenylene iodonium (DPI) and N-acetyl-L-cysteine (NAC), but not by AT2 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 AT1, resulting in effects on cardiomyocyte function such as hypertrophy.

Authors+Show Affiliations

Institute of Laboratory Medicine and Pathobiochemistry, Charité Medical Center, Humboldt University Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. shuling.wu@charite.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

16298685

Citation

Wu, Shuling, et al. "Activation of AP-1 Through Reactive Oxygen Species By Angiotensin II in Rat Cardiomyocytes." Free Radical Biology & Medicine, vol. 39, no. 12, 2005, pp. 1601-10.
Wu S, Gao J, Ohlemeyer C, et al. Activation of AP-1 through reactive oxygen species by angiotensin II in rat cardiomyocytes. Free Radic Biol Med. 2005;39(12):1601-10.
Wu, S., Gao, J., Ohlemeyer, C., Roos, D., Niessen, H., Köttgen, E., & Gessner, R. (2005). Activation of AP-1 through reactive oxygen species by angiotensin II in rat cardiomyocytes. Free Radical Biology & Medicine, 39(12), 1601-10.
Wu S, et al. Activation of AP-1 Through Reactive Oxygen Species By Angiotensin II in Rat Cardiomyocytes. Free Radic Biol Med. 2005 Dec 15;39(12):1601-10. PubMed PMID: 16298685.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of AP-1 through reactive oxygen species by angiotensin II in rat cardiomyocytes. AU - Wu,Shuling, AU - Gao,Jianping, AU - Ohlemeyer,Carsten, AU - Roos,Dirk, AU - Niessen,Hans, AU - Köttgen,Eckart, AU - Gessner,Reinhard, Y1 - 2005/08/24/ PY - 2005/01/13/received PY - 2005/07/19/revised PY - 2005/08/03/accepted PY - 2005/11/22/pubmed PY - 2006/3/8/medline PY - 2005/11/22/entrez SP - 1601 EP - 10 JF - Free radical biology & medicine JO - Free Radic Biol Med VL - 39 IS - 12 N2 - 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 (AT1) inhibitor CV-11974 as well as by the antioxidants diphenylene iodonium (DPI) and N-acetyl-L-cysteine (NAC), but not by AT2 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 AT1, resulting in effects on cardiomyocyte function such as hypertrophy. SN - 0891-5849 UR - https://www.unboundmedicine.com/medline/citation/16298685/Activation_of_AP_1_through_reactive_oxygen_species_by_angiotensin_II_in_rat_cardiomyocytes_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891-5849(05)00448-X DB - PRIME DP - Unbound Medicine ER -