Resveratrol inhibits MAPK activity and nuclear translocation in coronary artery smooth muscle: reversal of endothelin‐1 stimulatory effects

El‐Mowafy, Abdalla M.; White, Richard E.

doi:10.1016/s0014-5793(99)00541-4

Cited by 122 publications

(63 citation statements)

References 45 publications

(64 reference statements)

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“…Res was also reported to inhibit the activity of p38 MAPK signaling. For instance, Res inhibited MAPK activity in coronary artery smooth muscle (21). In addition, Res suppressed mouse skin tumor growth by inhibition of activated p38 MAPK (22).…”

Section: Discussionmentioning

confidence: 99%

Antitumor effect of resveratrol on chondrosarcoma cells via phosphoinositide 3-kinase/AKT and p38 mitogen-activated protein kinase pathways

Dai

Lei

Xie

et al. 2015

Molecular Medicine Reports

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Abstract. Chondrosarcoma is one of the most common types of primary bone cancer that develops in cartilage cells. Resveratrol (Res), a natural polyphenol compound isolated from various fruits, has a suppressive effect on various human malignancies. It has been shown that Res inhibits matrix metalloproteinase (MMP)-induced differentiation in chondrosarcoma cells. However, the effects of Res on cell proliferation, apoptosis and invasion of chondrosarcoma cells, as well as the underlying mechanisms, remain largely unknown. To the best of our knowledge, the present study showed for the first time that Res inhibited proliferation and induced apoptosis in chondrosarcoma cells in a dose-dependent manner. Furthermore, it was shown that Res also suppressed chondrosarcoma cell invasion in a dose-dependent manner, probably via the inhibition of MMP2 and MMP9 protein expression. Molecular mechanism investigations revealed that Res could inhibit the activity of phosphoinositide 3-kinase/AKT and p38 mitogen-activated protein kinase signaling pathways, which has been demonstrated to be important in the regulation of proliferation, apoptosis and invasion in various cancer cell types. In conclusion, this study suggests that Res may serve as a promising agent for the treatment of chondrosarcoma.

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Section: Discussionmentioning

confidence: 99%

Antitumor effect of resveratrol on chondrosarcoma cells via phosphoinositide 3-kinase/AKT and p38 mitogen-activated protein kinase pathways

Dai

Lei

Xie

et al. 2015

Molecular Medicine Reports

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“…27 In porcine coronary arteries, short-term treatment with resveratrol substantially inhibited mitogen-activated protein kinase activity and reduction in the phosphorylation of ERK1/2. 44 Recently, Haider et al 45 demonstrated that resveratrol inhibits angiotensin IIinduced vascular smooth muscle cell hypertrophy, possibly by interfering mainly with the ERK1/2 signaling pathway. One possible explanation for the inhibitory effect of resveratrol on strain-induced ET-1 gene expression may be its ability to attenuate ROS formation.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Cyclic Strain-Induced Endothelin-1 Gene Expression by Resveratrol

et al. 2003

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Abstract-Resveratrol is a phytoestrogen naturally found in grapes and is among the major constituents of wine thought to have a cardioprotective effect. Endothelin-1 (ET-1) is a potent vasopressor synthesized by endothelial cells both in culture and in vivo. The aims of this study were to test the hypothesis that resveratrol may alter strain-induced ET-1 gene expression and to identify the putative underlying signaling pathways in endothelial cells. We show that resveratrol indeed potently inhibits strain-induced ET-1 secretion, ET-1 mRNA level, and ET-1 promoter activity. Resveratrol also inhibits strain-increased NADPH oxidase activity, reactive oxygen species formation, and extracellular signal-regulated kinases1/2 (ERK1/2) phosphorylation. Furthermore, pretreating cells with resveratrol or antioxidant N-acetyl-cysteine decreases strain-increased or hydrogen peroxide-increased ET-1 secretion, ET-1 promoter activity, and ET-1 mRNA and ERK1/2 phosphorylation. Using both the electrophoretic mobility shift assay and a reporter gene assay, resveratrol and N-acetyl-cysteine also attenuated the strain-stimulated activator protein-1 binding activity and activator protein-1 reporter activity. In summary, we demonstrate for the first time that resveratrol inhibits strain-induced ET-1 gene expression, partially by interfering with the ERK1/2 pathway through attenuation of reactive oxygen species formation. Thus, this study provides important new insights in the molecular pathways that may contribute to the proposed beneficial effects of resveratrol in the cardiovascular system. any epidemiological studies show a correlation between a low incidence of coronary heart disease and atherosclerosis and a moderate consumption of red wine. 1,2 The vasoprotective effect of red wine, also known as the "French paradox," is currently best exemplified by transresveratrol (trans-3,5,4Ј-hydroxystilbene). 3,4 Resveratrol has many biological activities, including protection from or reduction of the incidence of coronary heart disease. Resveratrol also has been found to protect the heart from ischemiareperfusion injury. 5 Antioxidant properties of resveratrol appear to be partly responsible for this activity. 5-9 Moreover, resveratrol was shown to relax aortic rings in rats through an endothelium-mediated enhancement of the nitric oxide (NO)-cGMP cascade. 10 Subsequent pharmacological studies indicate a direct relaxant effect of resveratrol on vascular smooth muscle that may exert beneficial effects in cardiovascular disease, though the mechanism of these effects is no known. 11 Recently, Orallo et al 12 demonstrated that the characteristic endothelium-dependent vasorelaxant effect of resveratrol in the rat aorta appeared to be caused by the inhibition of vascular NADH/NADPH oxidase and the subsequent decrease in the generation of basal cellular superoxide anions and, therefore, of NO biotransformation. However, little is known about the cellular/molecular mechanisms whereby resveratrol could protect against coronary heart disease. Indee...

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“…Numerous studies suggest that resveratrol modulates all of these pathways. [67][68][69][70] Although contradictory findings exist, the majority of studies agree that the hydroxystilbene activates the ERK1/2 pathways. For example, it has been reported that resveratrol up-regulates ERK1/2 in human neuroblastoma SH-SY5Y cells.…”

confidence: 99%

“…In addition, resveratrol seems capable of reversing the upregulation of ERK1/2 due to endothelin-1. 69 Nevertheless, although it has not been demonstrated in all the experimental models examined, a good consensus exists that resveratrol activates the RasgMAPK kinaseg MAPK signal transduction pathway. In some specific instance, the activation of this pathway might increase p53 expression and activity (by Ser15 phosphorylation) and, in turn, p53-dependent apoptosis.…”

confidence: 99%

Resveratrol: From Basic Science to the Clinic

Cucciolla¹,

Borriello²,

Oliva³

et al. 2007

Cell Cycle

157

102

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Plants produce an extraordinary array of low molecular mass natural products endowed with biological activity. Among these molecules, resveratrol (3,5,4'-trihydroxystilbene) has been identified as an inhibitor of carcinogenesis with a pleiotropic mode of action. Extensive literature on its anticancer activity, performed in cellular models, suggests a potential antiproliferative and apoptogenic use of the stilbene. Similarly, studies on implanted cancers and chemical-induced tumors confirm a potential chemotherapeutical interest of the compound. Moreover, recent intriguing studies have demonstrated, in mice, that the negative effects (insulin resistance and hyperglycemia) of a high-fat diet might be prevented by resveratrol treatment. Despite these promising observations, only few clinical trials have been performed on the compound due to the scarce interest of pharmaceutical industry. We suggest that resveratrol might be considered an interesting anticancer compound in association with more specific target-oriented drugs.

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Resveratrol inhibits MAPK activity and nuclear translocation in coronary artery smooth muscle: reversal of endothelin‐1 stimulatory effects

Cited by 122 publications

References 45 publications

Antitumor effect of resveratrol on chondrosarcoma cells via phosphoinositide 3-kinase/AKT and p38 mitogen-activated protein kinase pathways

Antitumor effect of resveratrol on chondrosarcoma cells via phosphoinositide 3-kinase/AKT and p38 mitogen-activated protein kinase pathways

Inhibition of Cyclic Strain-Induced Endothelin-1 Gene Expression by Resveratrol

Resveratrol: From Basic Science to the Clinic

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