Involvement of the endothelial DDAH/ADMA pathway in nitroglycerin tolerance: The role of ALDH-2

Zhang, Guogang; Shi, Ruizheng; Jiang, De-Jian; Chen, Yue-Rong; Jia-Chen,; Tang, Zhengyan; Bai, Yongping; Xiao, Hong-Bo; Li, Yuan‐Jian

doi:10.1016/j.lfs.2008.01.002

Cited by 19 publications

(13 citation statements)

References 34 publications

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“…They are broadly defined as oxygen‐containing chemical species with reactive chemical properties 51. ROS produced by a cell when stimulated by environmental stress or other factors are considered as potential signaling molecules 52. The increase of the ROS concentration in the cells may cause DNA damage, genetic instability, cellular injury and eventually trigger cell death.…”

Section: Resultsmentioning

confidence: 99%

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Plasma‐Induced Death of HepG2 Cancer Cells: Intracellular Effects of Reactive Species

Yan

Xiong

Zou

et al. 2011

Plasma Processes & Polymers

195

169

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Section: Resultsmentioning

confidence: 99%

“…It is also well known that the presence of nitrogen‐containing radicals is closely related to the oxidative stress produced by ROS 52. NO could be biosynthesized endogenously from L ‐arginine, oxygen and NADPH by various nitric oxide synthase (NOS) enzymes 53, 54.…”

Section: Resultsmentioning

confidence: 99%

Plasma‐Induced Death of HepG2 Cancer Cells: Intracellular Effects of Reactive Species

Yan

Xiong

Zou

et al. 2011

Plasma Processes & Polymers

195

169

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“…Hsp90 has been shown to interact with a number of proteins that are required for efficient NO biosynthesis, including eNOS [43] and soluble guanylate cyclase [43]. Further, the chaperone activity of Hsp90 is ATP dependent.…”

Section: Discussionmentioning

confidence: 99%

Preserving mitochondrial function prevents the proteasomal degradation of GTP cyclohydrolase I

Sharma

Sun

Kumar

et al. 2012

Free Radical Biology and Medicine

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The development of pulmonary hypertension is a common accompaniment of congenital heart disease (CHD) with increased pulmonary blood flow. Our recent evidence suggests that asymmetric dimethylarginine (ADMA)-induced mitochondrial dysfunction causes endothelial nitric oxide synthase (eNOS) uncoupling secondary to a proteasome-dependent degradation of GTP cyclohydrolase I (GCH1) that results in a decrease in the NOS co-factor, tetrahydrobiopterin (BH4). Decreases in NO signaling are thought to be an early hallmark of endothelial dysfunction. As L-carnitine plays an important role in maintaining mitochondrial function in this study we examined the protective mechanisms and the therapeutic potential of L-carnitine on NO signaling in pulmonary arterial endothelial cells (PAEC) and in a lamb model of CHD and increased pulmonary blood flow (Shunt). Acetyl L-carnitine (ALC) attenuated the ADMA-mediated proteasomal degradation of GCH1. This preservation was associated with a decrease in the association of GCH1 with the Hsp70 and the C-terminus of Hsp70-interacting protein (CHIP) and a decrease in its ubiquitination. This in turn prevented the decrease in BH4 levels induced by ADMA and preserved NO signaling. Treatment of Shunt lambs with L-carnitine also reduced GCH1/CHIP interactions, attenuated the ubiquitination and degradation of GCH1, and increased BH4 levels compared to vehicle treated Shunt lambs. The increases in BH4 were associated with decreased NOS uncoupling and enhanced NO generation. Thus, we conclude that L-carnitine may have a therapeutic potential in the treatment of pulmonary hypertension in children with CHD with increased pulmonary blood flow.

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“…The concentration of TNF- α used to induce apoptosis in the present study was chosen on the basis of our previous studies [13], which demonstrated that TNF- α at the dose of 40 ng/mL could significantly induce ECs apoptosis. The concentration of NTG adopted is according to the studies [20, 21], which demonstrated that NTG at the dose of 10 μ M could induce nitrate tolerance. The choice of concentration of PKC- β 2 inhibitor was based on that 1 μ M CGP53353 could selectively inhibit PKC- β 2 activation in our previous study [22].…”

Section: Methodsmentioning

confidence: 99%

Nitroglycerine-Induced Nitrate Tolerance Compromises Propofol Protection of the Endothelial Cells against TNF-α: The Role of PKC-β₂and NADPH Oxidase

Lei

Liu

et al. 2013

Oxidative Medicine and Cellular Longevity

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Continuous treatment with organic nitrates causes nitrate tolerance and endothelial dysfunction, which is involved with protein kinase C (PKC) signal pathway and NADPH oxidase activation. We determined whether chronic administration with nitroglycerine compromises the protective effects of propofol against tumor necrosis factor (TNF-) induced toxicity in endothelial cells by PKC-β 2 dependent NADPH oxidase activation. Primary cultured human umbilical vein endothelial cells were either treated or untreated with TNF-α (40 ng/mL) alone or in the presence of the specific PKC-β 2 inhibitor CGP53353 (1 μM)), nitroglycerine (10 μM), propofol (100 μM), propofol plus nitroglycerin, or CGP53353 plus nitroglycerine, respectively, for 24 hours. TNF-α increased the levels of superoxide, Nox (nitrate and nitrite), malondialdehyde, and nitrotyrosine production, accompanied by increased protein expression of p-PKC-β 2, gP91phox, and endothelial cell apoptosis, whereas all these changes were further enhanced by nitroglycerine. CGP53353 and propofol, respectively, reduced TNF-α induced oxidative stress and cell toxicity. CGP53353 completely prevented TNF-α induced oxidative stress and cell toxicity in the presence or absence of nitroglycerine, while the protective effects of propofol were neutralized by nitroglycerine. It is concluded that nitroglycerine comprises the protective effects of propofol against TNF-α stimulation in endothelial cells, primarily through PKC-β 2 dependent NADPH oxidase activation.

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Involvement of the endothelial DDAH/ADMA pathway in nitroglycerin tolerance: The role of ALDH-2

Cited by 19 publications

References 34 publications

Plasma‐Induced Death of HepG2 Cancer Cells: Intracellular Effects of Reactive Species

Plasma‐Induced Death of HepG2 Cancer Cells: Intracellular Effects of Reactive Species

Preserving mitochondrial function prevents the proteasomal degradation of GTP cyclohydrolase I

Nitroglycerine-Induced Nitrate Tolerance Compromises Propofol Protection of the Endothelial Cells against TNF-α: The Role of PKC-β₂and NADPH Oxidase

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Involvement of the endothelial DDAH/ADMA pathway in nitroglycerin tolerance: The role of ALDH-2

Cited by 19 publications

References 34 publications

Plasma‐Induced Death of HepG2 Cancer Cells: Intracellular Effects of Reactive Species

Plasma‐Induced Death of HepG2 Cancer Cells: Intracellular Effects of Reactive Species

Preserving mitochondrial function prevents the proteasomal degradation of GTP cyclohydrolase I

Nitroglycerine-Induced Nitrate Tolerance Compromises Propofol Protection of the Endothelial Cells against TNF-α: The Role of PKC-β2and NADPH Oxidase

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Product

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Nitroglycerine-Induced Nitrate Tolerance Compromises Propofol Protection of the Endothelial Cells against TNF-α: The Role of PKC-β₂and NADPH Oxidase