H2O2 but not $${\hbox{O}_{2}^{-}}$$ elevated by oxidized LDL enhances human aortic smooth muscle cell proliferation

Yin, Chi-Chao; Huang, Kuang-Tse

doi:10.1007/s11373-006-9132-4

Cited by 24 publications

(13 citation statements)

References 44 publications

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“…Though it is clear that increased ROS levels are crucial to stimulating VSMC proliferation and migration, there is debate as to whether O 2 •− , H 2 O 2 , or both are the primary species responsible. Yin and Huang suggested that increased H 2 O 2 levels mediated by stimulation of both NOX1 and SOD accelerate VSMC proliferation [42]. However, other reports show that increasing O 2 •− production via stimulation of NOX1 is sufficient to drive VSMC proliferation [14,15,43].…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide inhibits neointimal hyperplasia following vascular injury via differential, cell-specific modulation of SOD-1 in the arterial wall

Bahnson¹,

Koo²,

Cantú‐Medellín³

et al. 2015

Nitric Oxide

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Superoxide (O2•−) promotes neointimal hyperplasia following arterial injury. Conversely, nitric oxide (•NO) inhibits neointimal hyperplasia through various cell-specific mechanisms, including redox regulation. What remains unclear is whether •NO exerts cell-specific regulation of the vascular redox environment following arterial injury to inhibit neointimal hyperplasia. Therefore, the aim of the present study was to assess whether •NO exerts cell-specific, differential modulation of O2•− levels throughout the arterial wall, establish the mechanism of such modulation, and determine if it regulates •NO-dependent inhibition of neointimal hyperplasia. In vivo, •NO increased superoxide dismutase-1 (SOD-1) levels following carotid artery balloon injury in a rat model. In vitro, •NO increased SOD-1 levels in vascular smooth muscle cells (VSMC), but had no effect on SOD-1 in endothelial cells or adventitial fibroblasts. This SOD-1 increase was associated with an increase in sod1 gene expression, increase in SOD-1 activity, and decrease in O2•− levels. Lastly, to determine the role of SOD-1 in •NO-mediated inhibition of neointimal hyperplasia, we performed the femoral artery wire injury model in wild type and SOD-1 knockout (KO) mice, with and without •NO. Interestingly, •NO inhibited neointimal hyperplasia only in wild type mice, with no effect in SOD-1 KO mice. In conclusion, these data show the cell-specific modulation of O2•− by •NO through regulation of SOD-1 in the vasculature, highlighting its importance on the inhibition of neointimal hyperplasia. These results also shed light into the mechanism of •NO-dependent redox balance, and suggest a novel VSMC redox target to prevent neointimal hyperplasia.

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Section: Discussionmentioning

confidence: 99%

Nitric oxide inhibits neointimal hyperplasia following vascular injury via differential, cell-specific modulation of SOD-1 in the arterial wall

Bahnson¹,

Koo²,

Cantú‐Medellín³

et al. 2015

Nitric Oxide

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“…Studies have demonstrated regression or a lower degree of atherosclerosis in experimental animals prone to the development of atherosclerosis, especially in LDLr −/− and ApoE −/− mice subjected to different benefits have been demonstrated by others 40,41) . The co-expression of CAT is important to decrease the proliferation of smooth muscle cells induced by oxLDL 42) . In addition, hydrogen peroxide increases the proliferation of these cells, resulting in an increased atherosclerotic process, but in the presence of CAT such proliferation does not occur 42) .…”

Section: Discussionmentioning

confidence: 99%

“…The co-expression of CAT is important to decrease the proliferation of smooth muscle cells induced by oxLDL 42) . In addition, hydrogen peroxide increases the proliferation of these cells, resulting in an increased atherosclerotic process, but in the presence of CAT such proliferation does not occur 42) . In the present study the low-intensity exercise training protocol induced a significant increase in GPx activity.…”

Section: Discussionmentioning

confidence: 99%

Improvements of Atherosclerosis and Hepatic Oxidative Stress are Independent of Exercise Intensity in LDLr<sup>-/-</sup> Mice

Teodoro

Natali²,

Fernandes³

et al. 2012

J Atheroscler Thromb

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) and G3 (0.014±0.001 cm 2 ) presented lower aortic fat deposition than G1 (0.039±0.005 cm 2 ). G2 and G3 exhibited higher HDL-C, TG and CAT activity, but lower lipid peroxidation and carbonyl protein than G1. SOD values were higher in G3 than G2 and G1, and GPx was higher in G2 than in G3 and G1. Conclusions: Our protocols of low-and moderate-intensity aerobic exercise training (30 min daily for 8 weeks) induced similar benefits in LDLr −/− mice with atherosclerosis.J Atheroscler Thromb, 2012; 19:904-911.

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“…Nox1 is activated or upregulated in VSMCs treated with AngII, LDL, or AGEs1, 25, 26. Nox1 overexpression increases serum-induced proliferation and PDGF-induced migration in VSMCs 27.…”

Section: Nox1mentioning

confidence: 99%

NADPH Oxidases: Functions and Pathologies in the Vasculature

Lassègue

Griendling

2010

ATVB

529

520

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Abstract-Reactive oxygen species are ubiquitous signaling molecules in biological systems. Four members of the NADPH oxidase (Nox) enzyme family are important sources of reactive oxygen species in the vasculature: Nox1, Nox2, Nox4, and Nox5. Signaling cascades triggered by stresses, hormones, vasoactive agents, and cytokines control the expression and activity of these enzymes and of their regulatory subunits, among which p22phox, p47phox, Noxa1, and p67phox are present in blood vessels. Vascular Nox enzymes are also regulated by Rac, ClC-3, Poldip2, and protein disulfide isomerase. Multiple Nox subtypes, simultaneously present in different subcellular compartments, produce specific amounts of superoxide, some of which is rapidly converted to hydrogen peroxide. The identity and location of these reactive oxygen species, and of the enzymes that degrade them, determine their downstream signaling pathways. Nox enzymes participate in a broad array of cellular functions, including differentiation, fibrosis, growth, proliferation, apoptosis, cytoskeletal regulation, migration, and contraction. They are involved in vascular pathologies such as hypertension, restenosis, inflammation, atherosclerosis, and diabetes. As our understanding of the regulation of these oxidases progresses, so will our ability to alter their functions and associated pathologies. Key Words: atherosclerosis Ⅲ blood vessels Ⅲ hypertension Ⅲ NADPH oxidase Ⅲ reactive oxygen species O ur knowledge of the signaling role of reactive oxygen species (ROS) in vascular physiology and pathophysiology has expanded tremendously in the past 15 years. NADPH oxidases (Nox) have emerged as major sources of ROS in the vasculature, multiple Nox subtypes have been cloned and analyzed structurally and functionally, and the relationship of Nox enzymes to signaling pathways, cellular function, and vascular disease has begun to be investigated.The Nox family consists of 7 catalytic homologues, 4 of which (Nox1, Nox2, Nox4, and Nox5) are found in the vasculature. These enzymes transfer electrons from NADPH to molecular oxygen, thus producing superoxide (O 2 ⅐Ϫ ). Because O 2 ⅐Ϫ does not readily cross membranes and is short-lived, its effect is mostly local. Depending on Nox subcellular location, O 2 ⅐Ϫ is released either inside organelles or extracellularly, with corresponding internal signaling or paracrine effects. Superoxide dismutase rapidly converts O 2 ⅐Ϫ to longer-lasting and membrane-diffusible H 2 O 2 , thus modifying the signal and expanding its range of action. Whereas some effects of Nox enzymes, such as inactivation of nitric oxide (NO ⅐ ) in blood pressure regulation, are mediated directly by O 2 ⅐Ϫ , many are instead attributable to protein modification by H 2 O 2 , including growth-related signal transduction in vascular smooth muscle cells (VSMC).In this brief review, we discuss our current understanding of vascular NADPH oxidases, especially their roles in physiology and disease. We first describe each oxidase separately, before presenting an overview of...

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H2O2 but not $${\hbox{O}_{2}^{-}}$$ elevated by oxidized LDL enhances human aortic smooth muscle cell proliferation

Cited by 24 publications

References 44 publications

Nitric oxide inhibits neointimal hyperplasia following vascular injury via differential, cell-specific modulation of SOD-1 in the arterial wall

Nitric oxide inhibits neointimal hyperplasia following vascular injury via differential, cell-specific modulation of SOD-1 in the arterial wall

Improvements of Atherosclerosis and Hepatic Oxidative Stress are Independent of Exercise Intensity in LDLr<sup>-/-</sup> Mice

NADPH Oxidases: Functions and Pathologies in the Vasculature

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