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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.

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Authors+Show Affiliations

Wu S
Institute of Laboratory Medicine and Pathobiochemistry, Charité Medical Center, Humboldt University Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. shuling.wu@charite.de
Gao J
No affiliation info available
Ohlemeyer C
No affiliation info available
Roos D
No affiliation info available
Niessen H
No affiliation info available
Köttgen E
No affiliation info available
Gessner R
No affiliation info available

MeSH

AcetylcysteineAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsAntioxidantsBenzimidazolesBiphenyl CompoundsCells, CulturedDose-Response Relationship, DrugHL-60 CellsHeart VentriclesHumansMyocytes, CardiacNADPH OxidasesOnium CompoundsOxidation-ReductionRatsRats, WistarReactive Oxygen SpeciesReceptor, Angiotensin, Type 1TetrazolesTime FactorsTranscription Factor AP-1

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 -