Cigarette smoke exposure impairs VEGF-induced endothelial cell migration: Role of NO and reactive oxygen species

Michaud, Sophie; Dussault, Sylvie; Groleau, Jessika; Haddad, Peter; Rivard, Alain

doi:10.1016/j.yjmcc.2006.05.004

Cited by 101 publications

(108 citation statements)

References 41 publications

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“…26 NO production was determined indirectly by measuring the concentration of the stable end products nitrate and nitrite using a commercial kit (R&D systems Inc) based on the Griess reaction. 18 …”

Section: Plasma Antioxidant Potential and No Releasementioning

confidence: 99%

“…18 CSE was applied to mouse aortic endothelial cells or EPCs in culture for 16 hours within 30 minutes of preparation to obtain a final concentration of 10%. This concentration corresponds approximately to exposure associated with smoking 1.5 pack per day.…”

Section: Preparation Of Cigarette Smoke Extractsmentioning

confidence: 99%

“…This concentration corresponds approximately to exposure associated with smoking 1.5 pack per day. 18 …”

Section: Preparation Of Cigarette Smoke Extractsmentioning

confidence: 99%

“…16 However, excessive production of ROS leads to cellular toxicity and has been associated with impaired angiogenesis in different models. 17,18 A major source of ROS in the vessel wall is the family of membrane-associated NADPH oxidases. 19,20 NADPH oxidase consists of a membrane-localized cytochrome b558 composed of gp91 phox (or Nox2) and p22 phox and the cytosolic components p47 phox and p67 phox .…”

mentioning

confidence: 99%

“…14 We also recently demonstrated that cigarette smoke exposure impairs VEGFdependent angiogenesis, and that this is at least partly attributable to the generation of ROS and the inhibition of NO bioactivity. 18 In the current study, to mimic a clinical situation of increased oxidative stress, animals were exposed to cigarette smoke before and after the surgical induction of hindlimb ischemia. Our aim was to investigate the role of Nox2-containing NADPH oxidase for the modulation of ischemia-induced neovascularization in conditions of increased oxidative stress, and to identify potential mechanisms involved in this pathophysiology.…”

mentioning

confidence: 99%

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Nox2-Containing NADPH Oxidase Deficiency Confers Protection From Hindlimb Ischemia in Conditions of Increased Oxidative Stress

Haddad

Dussault

Groleau

et al. 2009

ATVB

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Objective-Because Nox2-containing NADPH oxidase is a major source of ROS in the vasculature, we investigated its potential role for the modulation of ischemia-induced neovascularization in conditions of increased oxidative stress. Methods and Results-To mimic a clinical situation of increased oxidative stress, mice were exposed to cigarette smoke before and after the surgical induction of hindlimb ischemia. Nox2 expression and oxidative stress in ischemic tissues were significantly increased in wild-type mice, but not in mice deficient for the Nox2-containing NADPH oxidase (Nox2 Ϫ/Ϫ ). Nox2 Ϫ/Ϫ mice demonstrated faster blood flow recovery, increased capillary density in ischemic muscles, and improved endothelial progenitor cell functional activities compared to Nox2 ϩ/ϩ mice. In addition, Nox2 deficiency was associated with increased antioxidant and nitrite concentrations in plasma, together with a preserved expression of eNOS in ischemic tissues. In vitro, Nox2Ϫ/Ϫ endothelial cells exhibit resistance against superoxide induction and improved VEGF-dependent angiogenic activities compared to Nox2 ϩ/ϩ endothelial cells. Importantly, the beneficial effects of Nox2 deficiency on neovascularization in vitro and in vivo were lost after treatment with the NO inhibitor L-NAME. Conclusions-Nox2-containing NADPH oxidase deficiency protects against ischemia in conditions of increased oxidative stress. The mechanism involves improved neovascularization through a reduction of ROS formation, preserved activation of the VEGF/NO angiogenic pathway, and improved functional activities of endothelial progenitor cells.

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Section: Plasma Antioxidant Potential and No Releasementioning

confidence: 99%

Section: Preparation Of Cigarette Smoke Extractsmentioning

confidence: 99%

“…This concentration corresponds approximately to exposure associated with smoking 1.5 pack per day. 18 …”

Section: Preparation Of Cigarette Smoke Extractsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Nox2-Containing NADPH Oxidase Deficiency Confers Protection From Hindlimb Ischemia in Conditions of Increased Oxidative Stress

Haddad

Dussault

Groleau

et al. 2009

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Gastroschisis: A gene–environment model involving the VEGF–NOS3 pathway

Lammer¹,

Iovannisci²,

Tom

et al. 2008

American J of Med Genetics Pt C

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Gastroschisis is a severe major malformation in which an infant is delivered with a portion of intestines and possible other abdominal organs extruding through a defect in the abdominal wall, usually to the right of the umbilical cord. Etiologies of gastroschisis are largely unknown, and even its pathogenesis is poorly understood. Several recent epidemiological studies have identified interactions between maternal smoking during pregnancy, genetic variants of endothelial nitric oxide synthase, and risk for gastroschisis. We present a brief review of the endothelial nitric oxide synthase pathway and its relationship to vasculogenesis, suggesting that disruption of this pathway by environmental exposures or by genetic variation may represent one pathogenetic model for gastroschisis.

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Tobacco exposure and wound healing in head and neck surgical wounds

et al. 2017

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Objective Smoking impairs wound healing, yet the underlying pathophysiological mechanisms are unclear. We evaluated tobacco-altered healing in head and neck surgery by studying the association between biomarkers and tobacco exposure, as well as cutaneous perfusion by smoking status. Study Design Prospective cohort study, tertiary/academic care center, 2011 to present. Methods Patients who required head and neck surgery were enrolled prospectively. Postsurgical drain fluid was collected 24 hours postoperatively. Biomarkers associated with postulated mechanisms of smoking-impaired healing were assayed. These included interleukin-1, -6, and -8; tumor necrosis factor- alpha; transforming growth factor-beta; epidermal growth factor (EGF); basic fibroblastic growth factor (bFGF); C-reactive protein; vascular endothelial growth factor; soluble FMS-like tyrosine kinase-1 (sFLT-1); and placental growth factor. Tobacco exposure and clinical outcomes were recorded. Two sample two-sided t tests evaluated the differences in cytokine levels by tobacco exposure. In a second cohort, cutaneous vascular assessment via indocyanine green angiography was compared by smoking status. Results Twenty-eight patients were enrolled with drain fluid collection. Twenty-one subjects were current/former smokers, whereas seven were never smokers. EGF was higher in never smokers than smokers in a statistically significant manner (P = 0.030). Likewise, sFLT-1 was significantly higher in never smokers (P = 0.011). Cutaneous angiography revealed nonsmokers to have significantly higher cutaneous perfusion than smokers. Conclusion In this head and neck surgical cohort, significantly higher EGF and sFLT-1 levels in wound fluid were associated with never smoking, suggesting that smoking has adverse effects on the inflammatory phase of wound healing. Cutaneous angiography supports the detrimental effect of smoking on skin perfusion. These findings suggest the need for further study as well as therapeutic targets for smokers undergoing surgery.

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Cigarette smoke exposure impairs VEGF-induced endothelial cell migration: Role of NO and reactive oxygen species

Cited by 101 publications

References 41 publications

Nox2-Containing NADPH Oxidase Deficiency Confers Protection From Hindlimb Ischemia in Conditions of Increased Oxidative Stress

Nox2-Containing NADPH Oxidase Deficiency Confers Protection From Hindlimb Ischemia in Conditions of Increased Oxidative Stress

Gastroschisis: A gene–environment model involving the VEGF–NOS3 pathway

Tobacco exposure and wound healing in head and neck surgical wounds

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