Ambient pressure upregulates nitric oxide synthase in a phosphorylated-extracellular regulated kinase– and protein kinase C–dependent manner

Vouyouka, Angela G.; Jiang, Yan; Rastogi, Ruchi; Basson, Marc D.

doi:10.1016/j.jvs.2006.06.033

Cited by 13 publications

(10 citation statements)

References 58 publications

(84 reference statements)

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“…New findings have shown the importance of crosstalk between PI3K/Akt and MAPK pathways. The regulatory interaction between components of Akt and MAPK cascades and NO synthesis by endothelial cells has been well documented [47]. Our results show that Akt, ERK and p38 may be involved in eNOS phosphorylation induced by olive oil polyphenols.…”

Section: Discussionsupporting

confidence: 61%

Polyphenol fraction of extra virgin olive oil protects against endothelial dysfunction induced by high glucose and free fatty acids through modulation of nitric oxide and endothelin-1

et al. 2014

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Epidemiological and clinical studies have reported that olive oil reduces the incidence of cardiovascular disease. However, the mechanisms involved in this beneficial effect have not been delineated. The endothelium plays an important role in blood pressure regulation through the release of potent vasodilator and vasoconstrictor agents such as nitric oxide (NO) and endothelin-1 (ET-1), respectively, events that are disrupted in type 2 diabetes. Extra virgin olive oil contains polyphenols, compounds that exert a biological action on endothelial function. This study analyzes the effects of olive oil polyphenols on endothelial dysfunction using an in vitro model that simulates the conditions of type 2 diabetes. Our findings show that high glucose and linoleic and oleic acids decrease endothelial NO synthase phosphorylation, and consequently intracellular NO levels, and increase ET-1 synthesis by ECV304 cells. These effects may be related to the stimulation of reactive oxygen species production in these experimental conditions. Hydroxytyrosol and the polyphenol extract from extra virgin olive oil partially reversed the above events. Moreover, we observed that high glucose and free fatty acids reduced NO and increased ET-1 levels induced by acetylcholine through the modulation of intracellular calcium concentrations and endothelial NO synthase phosphorylation, events also reverted by hydroxytyrosol and polyphenol extract. Thus, our results suggest a protective effect of olive oil polyphenols on endothelial dysfunction induced by hyperglycemia and free fatty acids.

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Section: Discussionsupporting

confidence: 61%

Polyphenol fraction of extra virgin olive oil protects against endothelial dysfunction induced by high glucose and free fatty acids through modulation of nitric oxide and endothelin-1

et al. 2014

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“…Xu et al (28) also reported that the anti-infarct effect of NO donor S-nitroso-N-acetyl penicillamine was mediated by NOS-induced phosphorylation and activation of ERK1/2 in isolated rat cardiomyocytes and the intact heart, suggesting that ERK activation was downsteam of NOS (28). However, other studies demonstrated that ERK activation is required for the induction of NOS (3,24). Philipp et al (16) also reported that ERK phosphorylation occurred upstream of NOS in achetylcholine-induced protection in the rabbit heart.…”

Section: Discussionmentioning

confidence: 98%

ERK phosphorylation mediates sildenafil-induced myocardial protection against ischemia-reperfusion injury in mice

Das

Salloum²,

Xi³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

125

100

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Sildenafil, a selective inhibitor of phosphodiesterase type 5, induces powerful protection against myocardial ischemia-reperfusion injury through activation of cGMP-dependent protein kinase (PKG). We further hypothesized that PKG-dependent activation of survival kinase ERK may play a causative role in sildenafil-induced cardioprotection via induction of endothelial nitric oxide synthase (eNOS)/inducible nitric oxide synthase (iNOS) and Bcl-2. Our results show that acute intracoronary infusion of sildenafil in Langendorff isolated mouse hearts before global ischemia-reperfusion significantly reduced myocardial infarct size (from 29.4 +/- 2.4% to 15.9 +/- 3.0%; P < 0.05). Cotreatment with ERK inhibitor PD98059 abrogated sildenafil-induced protection (31.8 +/- 4.4%). To further evaluate the role of ERK in delayed cardioprotection, mice were treated with sildenafil (ip) 24 h before global ischemia-reperfusion. PD98059 was administered (ip) 30 min before sildenafil treatment. Infarct size was reduced from 27.6 +/- 3.3% in controls to 7.1 +/- 1.5% in sildenafil-treated mice (P < 0.05). The delayed protective effect of sildenafil was also abolished by PD98059 (22.5 +/- 2.3%). Western blots revealed that sildenafil significantly increased phosphorylation of ERK1/2 and GSK-3beta and induced iNOS, eNOS, Bcl-2, and PKG activity in the heart 24 h after treatment. PD98059 inhibited the enhanced expression of iNOS, eNOS, and Bcl-2 and the phosphorylation of GSK-3beta. PD98059 had no effect on the sildenafil-induced activation of PKG. We conclude that these studies provide first direct evidence that PKG-dependent ERK phosphorylation is indispensable for the induction of eNOS/iNOS and Bcl-2 and the resulting cardioprotection by sildenafil.

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“…Co-cultures of rat aortic endothelial and SMCs exposed to 130-135 mmHg of pressure show that ECs inhibit SMC proliferation and promote apoptosis likely through NO-dependent paracrine signaling (Vouyouka et al, 2006). ECs have been found to release significant amounts of the anticoagulant and vasodilator prostacyclin (Tokunaga et al, 1989) and increase production of the MMP collagenase (Kato et al, 1994).…”

Section: Pulsatile Pressurementioning

confidence: 99%

Exogenous and endogenous force regulation of endothelial cell behavior

Califano

Reinhart‐King

2010

Journal of Biomechanics

110

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Ambient pressure upregulates nitric oxide synthase in a phosphorylated-extracellular regulated kinase– and protein kinase C–dependent manner

Cited by 13 publications

References 58 publications

Polyphenol fraction of extra virgin olive oil protects against endothelial dysfunction induced by high glucose and free fatty acids through modulation of nitric oxide and endothelin-1

Polyphenol fraction of extra virgin olive oil protects against endothelial dysfunction induced by high glucose and free fatty acids through modulation of nitric oxide and endothelin-1

ERK phosphorylation mediates sildenafil-induced myocardial protection against ischemia-reperfusion injury in mice

Exogenous and endogenous force regulation of endothelial cell behavior

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