Effects of Resveratrol on Endothelial Progenitor Cells and Their Contributions to Reendothelialization in Intima-injured Rats

J, Gu; Cq, Wang; Hh, Fan; Ding, Haiyan; Xl, Xie; Ym, Xu; By, Wang; Dj, Huang

doi:10.1097/01.fjc.0000211764.52012.e3

Cited by 65 publications

(27 citation statements)

References 36 publications

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“…While Zu, et al reported SIRT1 promotes proliferation of primary porcine aortic ECs measured by crystal violet [21], our results showed that the down-regulation of rat aortic EC proliferation is induced when SIRT1 is activated by either NSS or resveratrol, which is an activator doubled the rate of deacetylation by SIRT1 at about 11 µM [37]. Resveratrol increased the proliferative, migratory, and adhesive activities of endothelial progenitor cells [38]. A recent study showed that resveratrol inhibited cell proliferation in a time- and dose-dependent manner in cultured human aortic and pulmonary arterial ECs [39].…”

Section: Discussionmentioning

confidence: 96%

SIRT1 and Connexin40 Mediate the Normal Shear Stress-Induced Inhibition of the Proliferation of Endothelial Cells Co-Cultured with Vascular Smooth Muscle Cells

Yao¹,

Qi²,

Zhang³

et al. 2013

Cell Physiol Biochem

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Background: Shear stress imposed by blood flow directly impacts endothelial cells (ECs), which are simultaneously influenced by neighboring vascular smooth muscle cells (VSMCs). However, the mechanisms by which shear stress and VSMCs modulate EC proliferation remain to be elucidated. Methods: ECs, cultured alone or co-cultured with VSMCs, were subjected to a normal level of laminar shear stress (NSS) of 15 dyne/cm² or kept under static conditions by using a parallel-plate flow chamber system, respectively. Results: BrdU incorporation assay and flow cytometry revealed that NSS inhibited EC proliferation with or without VSMCs. Western blot analysis demonstrated that NSS down-regulated the expression of Connexin40 (Cx40) in both ECs cultured alone and ECs co-cultured with VSMCs, accompanied by the increased expression of SIRT1. Moreover, salermide, an inhibitor of SIRT1, as well as SIRT1-specifc siRNA transfection inhibited the effect of NSS on EC proliferation and Cx40 expression. In contrast, resveratrol, a SIRT1 activator, induced an alteration in ECs similar to the application of NSS. Conclusion: NSS inhibits the proliferation of ECs via SIRT1 and Cx40 in the presence or absence of VSMCs. The data suggest that NSS plays a protective role in vascular homeostasis by maintaining EC proliferation at a normal level.

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Section: Discussionmentioning

confidence: 96%

SIRT1 and Connexin40 Mediate the Normal Shear Stress-Induced Inhibition of the Proliferation of Endothelial Cells Co-Cultured with Vascular Smooth Muscle Cells

Yao¹,

Qi²,

Zhang³

et al. 2013

Cell Physiol Biochem

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“…Resveratrol liquid formulations were prepared using ethanol (Sigma) as a solvent. Concentrations were chosen to reflect the range of doses previously shown to induce differential cellular effects 20 and all conditions were run in triplicate. The expression of SIRT1 was analysed by real-time-reverse transcription polymerase chain reaction (real time RT-PCR) (Applied Biosystems, Foster City, California).…”

Section: Methodsmentioning

confidence: 99%

The effect of resveratrol on normal and osteoarthritic chondrocyte metabolism

Kim

Braun

Dragoo

2014

Bone & Joint Research

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BackgroundResveratrol is a polyphenolic compound commonly found in the skins of red grapes. Sirtuin 1 (SIRT1) is a human gene that is activated by resveratrol and has been shown to promote longevity and boost mitochondrial metabolism. We examined the effect of resveratrol on normal and osteoarthritic (OA) human chondrocytes.MethodsNormal and OA chondrocytes were incubated with various concentrations of resveratrol (1 µM, 10 µM, 25 µM and 50 µM) and cultured for 24, 48 or 72 hours or for six weeks. Cell proliferation, gene expression, and senescence were evaluated.ResultsSIRT1 was significantly upregulated in normal chondrocytes with resveratrol concentrations of 25 µM and 50 µM on both two- (2D) (both p = 0.001) and three-dimensional (3D) cultures (p = 0.008 and 0.001, respectively). It was significantly upregulated in OA chondrocytes treated with 10 µM, 25 µM and 50 µM resveratrol on 2D cultures (p = 0.036, 0.002 and 0.001, respectively) and at 50 µM concentration on 3D cultures (p = 0.001). At 72 hours, the expression of collagen (COL)-10, aggrecan (AGG), and runt-related transcription factor 2 (RUNX2) was significantly greater in both 25 µM (p = 0.011, 0.006 and 0.015, respectively) and 50 µM (p = 0.019, 0.004 and 0.002, respectively) resveratrol-treated normal chondrocyte cultures. In OA chondrocytes, expression of COL10 and RUNX2 was significantly greater in 25 µM (p = 0.004 and 0.024) and 50 µM (p = 0.004 and 0.019) cultures at 72 hours on 3D cultures.ConclusionsAt concentrations of 25 µM and/or 50 µM, resveratrol treatment significantly upregulates SIRT1 gene expression in normal and osteoarthritic chondrocytes. Resveratrol induces chondrocytes into a hypertrophic state through upregulation of COL1, COL10, and RUNX2.Cite this article: Bone Joint Res 2014;3:51–9.

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“…Regarding its cardioprotective role, NOS expression was shown to increase at 1 μM concentration while it was decreased at 60 nM (Gu et al, 2006). …”

Section: Administration Doses Routes and Bioavailability Of Resveramentioning

confidence: 99%

Resveratrol: French Paradox Revisited

et al. 2012

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Resveratrol is a polyphenol that plays a potentially important role in many disorders and has been studied in different diseases. The research on this chemical started through the “French paradox,” which describes improved cardiovascular outcomes despite a high-fat diet in French people. Since then, resveratrol has been broadly studied and shown to have antioxidant, anti-inflammatory, anti-proliferative, and anti-angiogenic effects, with those on oxidative stress possibly being most important and underlying some of the others, but many signaling pathways are among the molecular targets of resveratrol. In concert they may be beneficial in many disorders, particularly in diseases where oxidative stress plays an important role. The main focus of this review will be the pathways affected by resveratrol. Based on these mechanistic considerations, the involvement of resveratrol especially in cardiovascular diseases, cancer, neurodegenerative diseases, and possibly in longevity will be is addressed.

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Effects of Resveratrol on Endothelial Progenitor Cells and Their Contributions to Reendothelialization in Intima-injured Rats

Cited by 65 publications

References 36 publications

SIRT1 and Connexin40 Mediate the Normal Shear Stress-Induced Inhibition of the Proliferation of Endothelial Cells Co-Cultured with Vascular Smooth Muscle Cells

SIRT1 and Connexin40 Mediate the Normal Shear Stress-Induced Inhibition of the Proliferation of Endothelial Cells Co-Cultured with Vascular Smooth Muscle Cells

The effect of resveratrol on normal and osteoarthritic chondrocyte metabolism

Resveratrol: French Paradox Revisited

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