Extracellular Superoxide Dismutase Deficiency Exacerbates Pressure Overload–Induced Left Ventricular Hypertrophy and Dysfunction

Lu, Zhigang; Xu, Xin; Hu, Xinli; Zhu, Guangshuo; Zhang, Ping; Deel, Elza D. van; French, Joel P.; Fassett, John; Oury, Tim D.; Bache, Robert J.; Chen, Yingjie

doi:10.1161/hypertensionaha.107.098186

Cited by 101 publications

(119 citation statements)

References 34 publications

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“…47 Thus it is not surprising that in hypertension the increased production of reactive oxygen species (ROS) is associated with an increased production of peroxynitrite in the heart and coronary blood vessels. 47,48,[73][74][75] The production of peroxynitrite itself has an impact on several pathways of vasodilation including reduced prostaglandin synthesis and inhibition of K + channels. 8,76 Additionally peroxynitrite impairs NO production through oxidation of BH 4 , a NOS co-factor 8,[76][77][78] and also impairs the sGC-mediated response to NO.…”

Section: Nitric Oxide-mediated Vasomotor Function Of Isolated Coronarmentioning

confidence: 99%

Nitric oxide and coronary vascular endothelium adaptations in hypertension

Levy

Chung²,

Kroetsch

et al. 2009

VHRM

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This review highlights a number of nitric oxide (NO)-related mechanisms that contribute to coronary vascular function and that are likely affected by hypertension and thus become important clinically as potential considerations in prevention, diagnosis, and treatment of coronary complications of hypertension. Coronary vascular resistance is elevated in hypertension in part due to impaired endothelium-dependent function of coronary arteries. Several lines of evidence suggest that other NO synthase isoforms and dilators other than NO may compensate for impairments in endothelial NO synthase (eNOS) to protect coronary artery function, and that NO-dependent function of coronary blood vessels depends on the position of the vessel in the vascular tree. Adaptations in NOS isoforms in the coronary circulation to hypertension are not well described so the compensatory relationship between these and eNOS in hypertensive vessels is not clear. It is important to understand potential functional consequences of these adaptations as they will impact the efficacy of treatments designed to control hypertension and coronary vascular disease. Polymorphisms of the eNOS gene result in significant associations with incidence of hypertension, although mechanistic details linking the polymorphisms with alterations in coronary vasomotor responses and adaptations to hypertension are not established. This understanding should be developed in order to better predict those individuals at the highest risk for coronary vascular complications of hypertension. Greater endothelium-dependent dilation observed in female coronary arteries is likely related to endothelial Ca 2+ control and eNOS expression and activity. In hypertension models, the coronary vasculature has not been studied extensively to establish mechanisms for sex differences in NO-dependent function. Genomic and nongenomic effects of estrogen on eNOS and direct and indirect antioxidant activities of estrogen are discussed as potential mechanisms of interest in coronary circulation that could have implications for sex-and estrogen status-dependent therapy for hypertension and coronary dysfunction. The current review identifies some important basic knowledge gaps and speculates on the potential clinical relevance of hypertension adaptations in factors regulating coronary NO function.

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Section: Nitric Oxide-mediated Vasomotor Function Of Isolated Coronarmentioning

confidence: 99%

Nitric oxide and coronary vascular endothelium adaptations in hypertension

Levy

Chung²,

Kroetsch

et al. 2009

VHRM

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“…16 Echocardiography and Western blots were performed with methods as described previously. 17,18 For details, please see the online data supplement, available at http://hyper.ahajournals.org.…”

Section: Mice and Tac Proceduresmentioning

confidence: 99%

Ecto-5′-Nucleotidase Deficiency Exacerbates Pressure-Overload–Induced Left Ventricular Hypertrophy and Dysfunction

Fassett

et al. 2008

Hypertension

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Abstract-This study examined whether endogenous extracellular adenosine acts to facilitate the adaptive response of the heart to chronic systolic overload. To examine whether endogenous extracellular adenosine can protect the heart against pressure-overload-induced heart failure, transverse aortic constriction was performed on mice deficient in extracellular adenosine production as the result of genetic deletion of CD73.

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“…4,5) Extracellular-SOD (EC-SOD) is one of the SOD isozymes and plays a pivotal role in the regulation of redox homeostasis, particularly in extracellular spaces. [6][7][8] A previous study reported that the knockdown of EC-SOD exacerbated the progression of atherogenesis through the accumulation of foam cells in the neointima region 9) ; on the other hand, the overexpression of EC-SOD has been shown to suppress atherogenesis. 10) Therefore, maintaining the expression of EC-SOD at high levels in vessel walls may prevent the initiation and progression of vascular diseases.…”

mentioning

confidence: 99%

CoCl<sub>2</sub> Decreases EC-SOD Expression through Histone Deacetylation in COS7 Cells

Hattori

Kamiya

Hara

et al. 2016

Biological & Pharmaceutical Bulletin

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Extracellular-superoxide dismutase (EC-SOD), one of the SOD isozymes, is negatively regulated under hypoxic conditions, and decreases in its expression may exacerbate vascular diseases. Moreover, epigenetics, such as DNA methylation and histone modifications, are known to play a critical role in the progression of cancer, type 2 diabetes, and atherosclerosis. We previously investigated the involvement of reactive oxygen species (ROS) and p38 mitogen-activated protein kinase (MAPK) in decreases in EC-SOD expression in hypoxic COS7 cells; however, the role of epigenetics in this process currently remains unknown. In the present study, we demonstrated that the hypoxia mimetic cobalt chloride (CoCl 2 ) decreased histone acetylation levels, and a pretreatment with 4-phenyl butyric acid (PBA), an inhibitor of histone deacetylase, significantly suppressed CoCl 2 -elicited histone deacetylation and decreases in EC-SOD. We found that CoCl 2 -elicited decreases in EC-SOD were accompanied by reductions in histone H3 acetylation levels within its promoter region. Furthermore, luteolin, a well-known flavonoid, significantly suppressed the CoCl 2 -elicited accumulation of ROS, p38-MAPK activation, and histone deacetylation. Collectively, the results of the present study showed for the first time that CoCl 2 decreases the expression of EC-SOD through its deacetylation and luteolin may be one of the seed compounds that maintain redox homeostasis, even under hypoxic conditions.

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Extracellular Superoxide Dismutase Deficiency Exacerbates Pressure Overload–Induced Left Ventricular Hypertrophy and Dysfunction

Cited by 101 publications

References 34 publications

Nitric oxide and coronary vascular endothelium adaptations in hypertension

Nitric oxide and coronary vascular endothelium adaptations in hypertension

Ecto-5′-Nucleotidase Deficiency Exacerbates Pressure-Overload–Induced Left Ventricular Hypertrophy and Dysfunction

CoCl<sub>2</sub> Decreases EC-SOD Expression through Histone Deacetylation in COS7 Cells

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