Alcohol‐Induced Up‐Regulation of Fibrinolytic Activity and Plasminogen Activators in Human Monocytes

Tabengwa, Edlue M.; Wheeler, Crystal G.; Yancey, Dwana A.; Grenett, Hernan E.; Booyse, François M.

doi:10.1111/j.1530-0277.2002.tb02647.x

Cited by 21 publications

(5 citation statements)

References 43 publications

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“…tPA activity was also induced in the meninges ( Fig. 1 d and e), which is consistent with its up-regulation in nonneuronal cells by ethanol (28,29).…”

Section: Results Tpa Is Up-regulated By Ethanol and Ewsupporting

confidence: 83%

Ethanol-withdrawal seizures are controlled by tissue plasminogen activator via modulation of NR2B-containing NMDA receptors

Pawlak

Melchor²,

Matys³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

130

134

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Chronic ethanol abuse causes up-regulation of NMDA receptors, which underlies seizures and brain damage upon ethanol withdrawal (EW). Here we show that tissue-plasminogen activator (tPA), a protease implicated in neuronal plasticity and seizures, is induced in the limbic system by chronic ethanol consumption, temporally coinciding with up-regulation of NMDA receptors. tPA interacts with NR2B-containing NMDA receptors and is required for up-regulation of the NR2B subunit in response to ethanol. As a consequence, tPA-deficient mice have reduced NR2B, extracellular signal-regulated kinase 1͞2 phosphorylation, and seizures after EW. tPA-mediated facilitation of EW seizures is abolished by NR2B-specific NMDA antagonist ifenprodil. These results indicate that tPA mediates the development of physical dependence on ethanol by regulating NR2B-containing NMDA receptors.proteases ͉ excitotoxicity ͉ alcoholism

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“…tPA activity was also induced in the meninges ( Fig. 1 d and e), which is consistent with its up-regulation in nonneuronal cells by ethanol (28,29).…”

Section: Results Tpa Is Up-regulated By Ethanol and Ewsupporting

confidence: 83%

Ethanol-withdrawal seizures are controlled by tissue plasminogen activator via modulation of NR2B-containing NMDA receptors

Pawlak

Melchor²,

Matys³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

130

134

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“…1 Moderate alcohol increases clot lysis in vivo in a mouse model, by increasing the expression of tissue plasminogen activator (t-PA) and urokinase plasminogen activator (u-PA), 8 a response also detected in human monocytes. 9 In contrast to the effect of alcohol, a deficit in eNOS function raises plasma fibrinogen. 10,11 It has been shown that eNOS plays a key role in the process of thrombosis.…”

Section: Haemostatic Mechanismsmentioning

confidence: 98%

A central role of eNOS in the protective effect of wine against metabolic syndrome

Leighton

Miranda-Rottmann

Urquiaga

2006

Cell Biochem. Funct.

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The positive health effects derived from moderate wine consumption are pleiotropic. They appear as improvements in cardiovascular risk factors such as plasma lipids, haemostatic mechanisms, endothelial function and antioxidant defences. The active principles would be ethanol and mainly polyphenols. Results from our and other laboratories support the unifying hypothesis that the improvements in risk factors after red wine consumption are mediated by endothelial nitric oxide synthase (eNOS). Many genes are involved, but the participation of eNOS would be a constant feature. The metabolic syndrome is a cluster of metabolic risk factors associated with high risk of cardiovascular disease (CVD). The National Cholesterol Education Programmmes Adult Treatment Panel III (NCEPATP III) clinical definition of the metabolic syndrome requires the presence of at least three risk factors, from among abdominal obesity, high plasma triacylglycerols, low plasma HDL, high blood pressure and high fasting plasma glucose. The molecular mechanisms responsible for the metabolic syndrome are not known. Since metabolic syndrome apparently affects 10-30% of the population in the world, research on its pathogenesis and control is needed. The recent finding that eNOS knockout mice present a cluster of cardiovascular risk factors comparable to those of the metabolic syndrome suggests that defects in eNOS function may cause human metabolic syndrome. These mice are hypertensive, insulin resistant and dyslipidemic. Further support for a pathogenic role of eNOS comes from the finding in humans that eNOS polymorphisms associate with insulin resistance and diabetes, with hypertension, with inflammatory and oxidative stress markers and with albuminuria. So, the data sustain the hypothesis that eNOS enhancement should reduce metabolic syndrome incidence and its consequences. Therefore red wine, since it enhances eNOS function, should be considered as a potential tool for the control of metabolic syndrome. This hypothesis is supported by epidemiological observations and needs experimental validation in human intervention studies.

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“…The exact mechanisms by which excessive alcohol consumption decrease serum levels of the 7.8 kDa fragment of apo-AII and the 5.9 kDa fragment of ␣E chain of fibrinogen remain to be investigated. It is of note that alcohol-induced alteration of fibrinolytic activity has been shown in human monocytes [33].…”

Section: Surface Enhanced Laser Desorption/ionization Time-of-flight mentioning

confidence: 99%

Application of proteomic technologies to discover and identify biomarkers for excessive alcohol consumption: A review

Nomura

Tomonaga

Sogawa

et al. 2007

Journal of Chromatography B

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Alcohol‐Induced Up‐Regulation of Fibrinolytic Activity and Plasminogen Activators in Human Monocytes

Cited by 21 publications

References 43 publications

Ethanol-withdrawal seizures are controlled by tissue plasminogen activator via modulation of NR2B-containing NMDA receptors

Ethanol-withdrawal seizures are controlled by tissue plasminogen activator via modulation of NR2B-containing NMDA receptors

A central role of eNOS in the protective effect of wine against metabolic syndrome

Application of proteomic technologies to discover and identify biomarkers for excessive alcohol consumption: A review

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