Dose-Dependent Regulation of NAD(P)H Oxidase Expression by Angiotensin II in Human Endothelial Cells

Rueckschloss, Uwe; Quinn, Mark T.; Holtz, Juergen; Morawietz, Henning

doi:10.1161/01.atv.0000035392.38687.65

Cited by 192 publications

(68 citation statements)

References 51 publications

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“…Interestingly, earlier investigators have reported that angiotensin II induced oxidative stress in vascular cells, for example, demonstrating that angiotensin II stimulated the production of ROS in endothelial cells by up-regulating the subunits of NADPH oxidases (17,18). In the present study, we confirmed that angiotensin II -induced production of the O 2 À radical in prostate cancer cells, as shown in Fig.…”

Section: Discussionmentioning

confidence: 99%

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Angiotensin II Induces Oxidative Stress in Prostate Cancer

Uemura

Ishiguro

et al. 2008

Molecular Cancer Research

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Angiotensin II has been shown to be a cytokine especially acting as a growth factor. A local renin-angiotensin system has been identified in the prostate gland, and the physiologic function of angiotensin II seems to be similar in prostate cancer, as we previously reported. In the present study, we explored the biological role of angiotensin II in oxidative stress of prostate cancer cells. Activated Akt was determined, and the expression of oxidative stress-related proteins (p47phox, manganese superoxide dismutase 2, glutathione peroxidase) was examined by Western blotting in LNCaP cells, which were stimulated with angiotensin II and/or an angiotensin II receptor type 1 blocker, candesartan. To examine DNA damage induced by angiotensin II, 8-hydroxy-2 ¶-deoxyguanosine was determined, and Western blots were analyzed to detect checkpoint proteins including p53, Chk2, and cdc2. Immunocytochemical studies of inducible nitric oxide synthase and superoxide anion radical (O 2 À ) were done in LNCaP cells stimulated with angiotensin II. The phosphorylation of Akt was induced by angiotensin II treatment and inhibited by candesartan, as well as by LY294002, an inhibitor of phosphoinositide 3-kinase. Oxidative stress-related proteins were up-regulated by angiotensin II and inhibited by pretreatment with candesartan or catalase. The level of 8-hydroxy-2 ¶-deoxyguanosine was increased by angiotensin II and conversely decreased by candesartan. Immunocytochemical studies showed that angiotensin II enhanced an inflammatory marker, inducible nitric oxide synthase, and the production of O 2 À radical. The hypothesis that angiotensin II has the potential to induce oxidative stress, which may be implicated in carcinogenesis of the prostate gland through long-term exposure to chronic inflammation is proposed. (Mol Cancer Res 2008;6(2):250 -8)

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Section: Discussionmentioning

confidence: 99%

“…Of interest, many investigators have clarified that angiotensin II induces oxidative stress in vascular cells. Angiotensin II stimulates the production of ROS in endothelial cells by up-regulating the subunits of NAD + /NADP + (NADPH) oxidases (17,18).…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II Induces Oxidative Stress in Prostate Cancer

Uemura

Ishiguro

et al. 2008

Molecular Cancer Research

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“…8 Additionally, AT1 receptor antagonists have been shown to be antioxidant and vasoprotective in patients with coronary artery disease, in relation with downregulation of vascular NAD(P)H oxidase expression. 9 Treatment with either an angiotensin-converting enzyme inhibitor or an AT1 receptor antagonist resulted in lower levels of vascular O 2 Ϫ . The results of the present study by Bahlmann et al document that angiotensin receptor antagonists increase the number of EPCs in patient with type II diabetes mellitus.…”

Section: Angiotensin II Inflammation and Epcsmentioning

confidence: 99%

Beneficial Effects of Circulating Progenitor Endothelial Cells Activated by Angiotensin Receptor Antagonists

Lévy

2005

Hypertension

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“…Experimentos in vivo e in vitro, têm mostrado que a angiotensina II aumenta a formação de espécies reativas de oxigênio e a regulação da expressão proteica e de mRNA para subunidades de NAD(P)H oxidase, contribuindo, portanto, para a piora do estado oxidativo em indiví-duos com insuficiência cardíaca 55,56 .…”

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Insuficiência cardíaca e atividade física: o aumento de enzimas antioxidantes e a melhora da atividade nervosa simpática

Gonçalves

Valenti

Ferreira

et al. 2010

Arq. Bras. Ciên. Saúde

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ResumoA insuficiência cardíaca vem se tornando um problema cada vez maior em saúde pública, e uma das principais causas de internações hospitalares em todo o mundo.Mesmo com os progressos médicos e os avanços tecnológicos atuais, a prevalência da doença aumentou nas últimas cinco décadas. Estudos recentes com animais mostraram que existe uma relação entre hiperatividade simpática na insuficiência cardíaca e aumento do estresse oxidativo sistêmico e central. Este trabalho tem como objetivo analisar, por meio de revisão bibliográfica, os benefícios produzidos pela atividade física em pacientes portadores de insuficiência cardíaca. Foram revisados estudos relacionados ao estresse oxidativo, controle neural da circulação, insuficiência cardíaca e exercício físico entre outubro de 2009 e abril de 2010 nas bases de dados: Medline, Pubmed e Lilacs. As referências eram datadas de 1986 a 2010. Utilizaram-se os seguintes termos: "Oxidative Stress", "Chronic Heart Failure", "Baroreflex", "Nervous System" and "Exercise". Ratos com insuficiência cardíaca induzida possuem um aumento de espécies reativas de oxigênio na região rostroventrolateral do bulbo, assim como comprometimento na atividade simpática. Alguns estudos sugerem que a atividade física normaliza a atividade simpática por meio de seus mecanismos antioxidantes em seres humanos. Outro aspecto interessante é que a atividade física reduz os níveis plasmáticos de angiotensina II, regula a disfunção do baroreflexo arterial e promove o aumento de enzimas antioxidantes no músculo esquelético de pacientes com insuficiência cardíaca. Portanto, conclui-se que a atividade física é um regime terapêutico não-farmacológico de extrema importância para pacientes com insuficiência cardíaca.Palavras-chave: Insuficiência cardíaca; estresse oxidativo; exercício físico; sistema neural. AbstractHeart failure is an increasing problem in public health, and a major cause of hospitalization worldwide. Even with the medical progress and technological advances in the present, the prevalence of the disease increased in the last five decades. Recent animal studies have shown that there is a relationship between sympathetic hyperactivity in heart failure and increased oxidative stress, systemic and central. This paper aims to examine, through literature review, the benefits of physical activity in patients with heart failure. We reviewed studies related to oxidative stress, neural control of circulation, heart failure and exercise between October 2009 and April 2010, on the databases: Medline, Pubmed e Lilacs. The references dated from 1986 to 2010, and we used the following terms: "oxidative stress", "chronic heart failure", "baroreflex", "nervous system" and "exercise". Rats with induced heart failure have an increase of reactive oxygen species in the rostroventrolateral medula, and impairment of sympathetic activity. Some studies suggest that physical activity normalizes the sympathetic activity through its antioxidant mechanisms in the rostroventrolateral medulla. Some studies suggest that ...

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Dose-Dependent Regulation of NAD(P)H Oxidase Expression by Angiotensin II in Human Endothelial Cells

Cited by 192 publications

References 51 publications

Angiotensin II Induces Oxidative Stress in Prostate Cancer

Angiotensin II Induces Oxidative Stress in Prostate Cancer

Beneficial Effects of Circulating Progenitor Endothelial Cells Activated by Angiotensin Receptor Antagonists

Insuficiência cardíaca e atividade física: o aumento de enzimas antioxidantes e a melhora da atividade nervosa simpática

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