Requirement for Generation of H
            <sub>2</sub>
            O
            <sub>2</sub>
            for Platelet-Derived Growth Factor Signal Transduction

Sundaresan, Maitrayee; Yu, Zu Xi; Ferrans, Víctor J.; Irani, Kaikobad; Finkel, Toren

doi:10.1126/science.270.5234.296

Cited by 2,439 publications

(1,808 citation statements)

References 29 publications

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“…Administering ROS activates a wide variety of proteins in various pathways; for example, platelet-derived growth factor (PDGF), EGF, mitogen-activated protein kinase (MAPK), protein kinase C (PKC) and protein kinase B (PKB/Akt) signal-transduction pathways. H 2 O 2 generation during the activation of PDGF, transforming growth factor and EGF receptor signaling has also been well established (Sundaresan et al, 1995;Bae et al, 1997;Brar et al, 1999;Junn et al, 2000;Okuyama et al, 2001). The H 2 O 2 generated results in tyrosine phosphorylation of the receptor, which subsequently activates MAPK (Gamou and Shimizu, 1995).…”

Section: Intracellular Redox State and Cell Cycle Proteinsmentioning

confidence: 94%

A redox cycle within the cell cycle: ring in the old with the new

2006

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In recent years, the intracellular oxidation-reduction (redox) state has gained increasing attention as a critical mediator of cell signaling, gene expression changes and proliferation. This review discusses the evidence for a redox cycle (i.e., fluctuation in the cellular redox state) regulating the cell cycle. The presence of redox-sensitive motifs (cysteine residues, metal co-factors in kinases and phosphatases) in several cell cycle regulatory proteins indicate periodic oscillations in intracellular redox state could play a central role in regulating progression from G 0 /G 1 to S to G 2 and M cell cycle phases. Fluctuations in the intracellular redox state during cell cycle progression could represent a fundamental mechanism linking oxidative metabolic processes to cell cycle regulatory processes. Proliferative disorders are central to a variety of human pathophysiological conditions thought to involve oxidative stress. Therefore, a more complete understanding of redox control of the cell cycle could provide a biochemical rationale for manipulating aberrant cell proliferation.

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Section: Intracellular Redox State and Cell Cycle Proteinsmentioning

confidence: 94%

A redox cycle within the cell cycle: ring in the old with the new

2006

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“…Stimulation of growth factor receptors, toll like receptors (TLR), and cytokine receptors, also leads to the activation of signaling cascades that are regulated by hydrogen peroxide (H 2 O 2 ) as a result of activation of non-phagocytic oxidases (NOX), or dual oxidase (DUOX) (See Table 1) [18,19,[21][22][23][24]. The expression of multiple isoforms of these enzymes in a variety of tissues provides evidence that the deliberate production of low levels of oxidants is a feature of many cells [25].…”

Section: Oxidants As Modulators Of Signal Transductionmentioning

confidence: 99%

Redox-based regulation of signal transduction: Principles, pitfalls, and promises

Janssen–Heininger¹,

Mossman²,

Heintz³

et al. 2008

Free Radical Biology and Medicine

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698

652

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“…Among many agents, including cytokines, Ang II, and growth factors, PDGF is considered to be a primary stimulator of VSMC migration and proliferation, acting on the PDGF‐β receptor in medial SMCs and leading to neointimal growth 7, 20. Ang II– and PDGF‐BB–induced VSMC migration and proliferation in vitro are mediated via generation of ROS 6, 21. Ang II stimulates ROS production in VSMCs via activation of nicotinamide adenine dinucleotide phosphate (NADPH oxidase), which is dependent on arachidonic acid (AA) 22.…”

Section: Discussionmentioning

confidence: 99%

Cytochrome P450 1B1 Is Critical for Neointimal Growth in Wire‐Injured Carotid Artery of Male Mice

Mukherjee

Song

Estes

et al. 2018

JAHA

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BackgroundWe have reported that cytochrome P450 1B1 (CYP1B1), expressed in cardiovascular tissues, contributes to angiotensin II–induced vascular smooth muscle cell (VSMC) migration and proliferation and development of hypertension in various experimental animal models via generation of reactive oxygen species. This study was conducted to determine the contribution of CYP1B1 to platelet‐derived growth factor‐BB–induced VSMC migration and proliferation in vitro and to neointimal growth in vivo.Methods and Results VSMCs isolated from aortas of male Cyp1b1 +/+ and Cyp1b1 −/− mice were used for in vitro experiments. Moreover, carotid arteries of Cyp1b1 +/+ and Cyp1b1 −/− mice were injured with a metal wire to assess neointimal growth after 14 days. Platelet‐derived growth factor‐BB–induced migration and proliferation and H2O2 production were found to be attenuated in VSMCs from Cyp1b1 −/− mice and in VSMCs of Cyp1b1 +/+ mice treated with 4‐hydroxy‐2,2,6,6‐tetramethylpiperidin‐1‐oxyl, a superoxide dismutase and catalase mimetic. In addition, wire injury resulted in neointimal growth, as indicated by increased intimal area, intima/media ratio, and percentage area of restenosis, as well as elastin disorganization and adventitial collagen deposition in carotid arteries of Cyp1b1 +/+ mice, which were minimized in Cyp1b1 −/− mice. Wire injury also increased infiltration of inflammatory and immune cells, as indicated by expression of CD68+ macrophages and CD3+ T cells, respectively, in the injured arteries of Cyp1b1 +/+ mice, but not Cyp1b1 −/− mice. Administration of 4‐hydroxy‐2,2,6,6‐tetramethylpiperidin‐1‐oxyl attenuated neointimal growth in wire‐injured carotid arteries of Cyp1b1 +/+ mice.ConclusionsThese data suggest that CYP1B1‐dependent oxidative stress contributes to the neointimal growth caused by wire injury of carotid arteries of male mice.

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Requirement for Generation of H ₂ O ₂ for Platelet-Derived Growth Factor Signal Transduction

Cited by 2,439 publications

References 29 publications

A redox cycle within the cell cycle: ring in the old with the new

A redox cycle within the cell cycle: ring in the old with the new

Redox-based regulation of signal transduction: Principles, pitfalls, and promises

Cytochrome P450 1B1 Is Critical for Neointimal Growth in Wire‐Injured Carotid Artery of Male Mice

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Requirement for Generation of H 2 O 2 for Platelet-Derived Growth Factor Signal Transduction

Cited by 2,439 publications

References 29 publications

A redox cycle within the cell cycle: ring in the old with the new

A redox cycle within the cell cycle: ring in the old with the new

Redox-based regulation of signal transduction: Principles, pitfalls, and promises

Cytochrome P450 1B1 Is Critical for Neointimal Growth in Wire‐Injured Carotid Artery of Male Mice

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Requirement for Generation of H ₂ O ₂ for Platelet-Derived Growth Factor Signal Transduction