Reactive Oxygen Species and Age‐Related Genes p66Shc, Sirtuin, FoxO3 and Klotho in Senescence

Afanas’ev, Igor B.

doi:10.4161/oxim.3.2.11050

Cited by 21 publications

(11 citation statements)

References 65 publications

(73 reference statements)

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“…It was reported that the expression of p16, p21, p27, and p53 in primary cells treated with antiaging agents such as kinetin and selenium was significantly reduced [25]. It is considered that Sirt1 might allow the repair of oxidative stress-induced damage to the intracellular proteins [42]. This possibility is explained partly by the fact that EGCG could partially maintain the activity of Sirt1 and concomitantly stimulate p53 acetylation.…”

Section: Resultsmentioning

confidence: 99%

Preventive Effects of Epigallocatechin-3-O-Gallate against Replicative Senescence Associated with p53 Acetylation in Human Dermal Fibroblasts

Han

Lee

Kim

et al. 2012

Oxidative Medicine and Cellular Longevity

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Considering the various pharmacological activities of epigallocatechin-3-O-gallate (EGCG) including anticancer, and anti-inflammatory, antidiabetic, and so forth, relatively less attention has been paid to the antiaging effect of EGCG on primary cells. In this study, the preventive effects of EGCG against serial passage-induced senescence were investigated in primary cells including rat vascular smooth muscle cells (RVSMCs), human dermal fibroblasts (HDFs), and human articular chondrocytes (HACs). The involvement of Sirt1 and acetylated p53 was examined as an underlying mechanism for the senescence preventive activity of EGCG in HDFs. All cells were employed with the initial passage number (PN) between 3 and 7. For inducing senescence, the cells were serially passaged at the predetermined times and intervals in the absence or presence of EGCG (50 or 100 μM). Serial passage-induced senescence in RVSMCs and HACs was able to be significantly prevented at 50 μM EGCG, while in HDFs, 100 μM EGCG could significantly prevent senescence and recover their cell cycle progression close to the normal level. Furthermore, EGCG was found to prevent serial passage- and H2O2-induced senescence in HDFs by suppressing p53 acetylation, but the Sirt1 activity was unaffected. In addition, proliferating HDFs showed similar cellular uptake of FITC-conjugated EGCG into the cytoplasm with their senescent counterparts but different nuclear translocation of it from them, which would partly account for the differential responses to EGCG in proliferating versus senescent cells. Taking these results into consideration, it is suggested that EGCG may be exploited to craft strategies for the development of an antiaging or age-delaying agent.

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Section: Resultsmentioning

confidence: 99%

Preventive Effects of Epigallocatechin-3-O-Gallate against Replicative Senescence Associated with p53 Acetylation in Human Dermal Fibroblasts

Han

Lee

Kim

et al. 2012

Oxidative Medicine and Cellular Longevity

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“…In addition to their HDAC activity Sirt1/3 play an important role in many ROS-dependent gene/enzyme cascades under physiological and pathophysiological conditions [27][28][29]. Owing to principal role of Sirt1/3 in many biological processes we will consider some of them in this work.…”

Section: Ros Signaling In the Class III Histone Deacetylasesmentioning

confidence: 98%

Nucleophilic Mechanism of ROS/RNS Signaling in Cancer Epigenetic Modifications

Afanas¹,

Nemesio²

2012

Am. J. Biomed. Sci.

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It has been shown that cancer is characterized by enhanced oxidative stress. Therefore reactive oxygen and nitrogen species (ROS/RNS) signaling in epigenetic modifications of cancer cells might be even more important comparing to the other pathologies. It is known that ROS/RNS can change DNA methylation through the direct interaction with DNA molecules and by affecting the levels of DNA methyltransferases. ROS/RNS signaling also plays an important role in the mechanism of acetylation/deacetylation of histones by histone acetyltransferases (HAT) and histone deacetylases (HDAC). We suggest that ROS/RNS signaling in epigenetic processes proceeds by a nucleophilic mechanism of etherification and hydrolysis where free radicals superoxide and nitric oxide manifest their nucleophilic properties. As HDAC inhibitors are effective ROS producers, the enhanced oxidative stress might be at least partly responsible for their anticancer activity as epigenetic drugs.

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“…The functional link between emphysema and aging implied by the findings on regulation of Klotho and senescence marker protein-30 which are implicated in both of these processes (Afanas’ev, 2010; Koike et al, 2010; Sato et al, 2006; Suga et al, 2000). It remains to be known whether SIRT1 regulates these genes and proteins in response to CS exposure.…”

Section: Sirt1 As a Target For Inflammagingmentioning

confidence: 99%

SIRT1 as a therapeutic target in inflammaging of the pulmonary disease

Rahman

Kinnula

Gorbunova

et al. 2012

Preventive Medicine

102

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Objective Chronic inflammation and cellular senescence are intertwined in the pathogenesis of premature aging, which is considered as an important contributing factor in driving chronic obstructive pulmonary disease (COPD). SIRT1, a NAD+-dependent protein/histone deacetylase, regulates inflammation, senescence/aging, stress resistance, and DNA damage repair via deacetylating intracellular signaling molecules and chromatin histones. The present review describes the mechanism and regulation of SIRT1 by environmental agents/oxidants/reactive aldehydes and pro-inflammatory stimuli in lung inflammation and aging. The role of dietary polyphenols in regulation of SIRT1 in inflammaging is also discussed. Methods Analysis of current research findings on the mechanism of inflammation and senescence/aging (i.e., inflammaging) and their regulation by SIRT1 in premature aging of the lung. Results COPD is a disease of lung inflammaging, which is associated with the DNA damage response, transcription activation and chromatin modifications. SIRT1 regulates inflammaging via regulating FOXO3, p53, NF-κB, histones and various proteins involved in DNA damage and repair. Polyphenols and its analogs have been shown to activate SIRT1 although they have anti-inflammatory and antioxidant properties. Conclusions Targeting lung inflammation and cellular senescence as well as premature lung aging using pharmacological SIRT1 activators or polyphenols would be a promising therapeutic intervention for COPD/emphysema.

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Reactive Oxygen Species and Age‐Related Genes p66Shc, Sirtuin, FoxO3 and Klotho in Senescence

Cited by 21 publications

References 65 publications

Preventive Effects of Epigallocatechin-3-O-Gallate against Replicative Senescence Associated with p53 Acetylation in Human Dermal Fibroblasts

Preventive Effects of Epigallocatechin-3-O-Gallate against Replicative Senescence Associated with p53 Acetylation in Human Dermal Fibroblasts

Nucleophilic Mechanism of ROS/RNS Signaling in Cancer Epigenetic Modifications

SIRT1 as a therapeutic target in inflammaging of the pulmonary disease

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