SIRT1 activation mediates heat-induced survival of UVB damaged Keratinocytes

Calapre, Leslie; Gray, Elin S.; Kurdykowski, Sandrine; David, Anthony; Descargues, Pascal; Ziman, Mel

doi:10.1186/s12895-017-0060-y

Cited by 7 publications

(9 citation statements)

References 59 publications

(79 reference statements)

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“…Several studies have shown that heat stress promotes skin carcinogenesis [102][103][104]. The issue of subsequent action of UVB and heat on skin cancer was raised in the study conducted by Calapre et al [41]. The findings from the study are directly in line with previous findings on regulation of SIRT1 expression by UVR and high temperature [38,105].…”

Section: Sirtuin 1 Affects Ultraviolet Irradiation-related Skin Changsupporting

confidence: 80%

“…Recently, considerable effort has been put into exploring molecular mechanisms underlying the effect of SIRT1 on the UV-induced alterations in skin. Beyond increased oxidative stress resistance and enhanced NER repair system, sirtuin 1 reduces transcriptional activity of p53 and p16 proteins and its downstream pathways [40][41][42]44]. While generally cell survival is advantageous in terms of skin aging, chronic accumulation of damage and attenuation of p53-related cell cycle arrest may contribute to the survival of DNA damaged keratinocytes, and thus, skin carcinogenesis.…”

Section: Sirtuin 1 Affects Ultraviolet Irradiation-related Skin Changmentioning

confidence: 99%

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Sirtuin 1 and Skin: Implications in Intrinsic and Extrinsic Aging—A Systematic Review

Bielach-Bazyluk

Zbroch

Myśliwiec

et al. 2021

Cells

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Skin, as the outermost organ of the body, is constantly exposed to both intrinsic and extrinsic causative factors of aging. Intrinsic aging is related to compromised cellular proliferative capacity, and may be accelerated by harmful environmental influences with the greatest significance of ultraviolet radiation exposure, contributing not only to premature aging, but also to skin carcinogenesis. The overall skin cancer burden and steadily increasing global antiaging market provide an incentive for searching novel targets to improve skin resistance against external injury. Sirtuin 1, initially linked to extension of yeast and rodent lifespan, plays a key role in epigenetic modification of proteins, histones, and chromatin by which regulates the expression of genes implicated in the oxidative stress response and apoptosis. The spectrum of cellular pathways regulated by sirtuin 1 suggests its beneficial impact on skin aging. However, the data on its role in carcinogenesis remains controversial. The aim of this review was to discuss the relevance of sirtuin 1 in skin aging, in the context of intrinsic factors, related to genetic premature aging syndromes, as well as extrinsic modifiable ones, with the assessment of its future application. PubMed were searched from inception to 4 January 2021 for relevant papers with further search carried out on ClinicalTrials.gov. The systematic review included 46 eligible original articles. The evidence from numerous studies proves sirtuin 1 significance in both chronological and premature aging as well as its dual role in cancer development. Several botanical compounds hold the potential to improve skin aging symptoms.

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Section: Sirtuin 1 Affects Ultraviolet Irradiation-related Skin Changsupporting

confidence: 80%

Section: Sirtuin 1 Affects Ultraviolet Irradiation-related Skin Changmentioning

confidence: 99%

Sirtuin 1 and Skin: Implications in Intrinsic and Extrinsic Aging—A Systematic Review

Bielach-Bazyluk

Zbroch

Myśliwiec

et al. 2021

Cells

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“…Thus, human premature aging disorders are strongly associated with defects in DSBR, BER, and NER . Furthermore, repair of DNA damage is an energy demanding process and it is becoming increasingly evident that DNA damage and persistent DDR‐linked cellular stress leads to mitochondrial dysfunction and metabolic defects . The following paragraphs discuss the molecular mechanisms underlying this signaling and how it relates to cellular bioenergetics/energy homeostasis and the cellular abundance of ATP and NAD + .…”

Section: Dna Damage Response Pathwaysmentioning

confidence: 99%

“…Thus, human premature aging disorders are strongly associated with defects in DSBR, BER, and NER [14]. Furthermore, repair of DNA damage is an energy demanding process [15][16][17][18][19][20] and it is becoming increasingly evident that DNA damage and persistent DDR-linked cellular stress leads to mitochondrial dysfunction and metabolic defects [21].…”

Section: Dna Damage Response Pathwaysmentioning

confidence: 99%

Toward understanding genomic instability, mitochondrial dysfunction and aging

Fakouri

Demarest

et al. 2018

The FEBS Journal

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The biology of aging is an area of intense research, and many questions remain about how and why cell and organismal functions decline over time. In mammalian cells, genomic instability and mitochondrial dysfunction are thought to be among the primary drivers of cellular aging. This review focuses on the interrelationship between genomic instability and mitochondrial dysfunction in mammalian cells and its relevance to age‐related functional decline at the molecular and cellular level. The importance of oxidative stress and key DNA damage response pathways in cellular aging is discussed, with a special focus on poly (ADP‐ribose) polymerase 1, whose persistent activation depletes cellular energy reserves, leading to mitochondrial dysfunction, loss of energy homeostasis, and altered cellular metabolism. Elucidation of the relationship between genomic instability, mitochondrial dysfunction, and the signaling pathways that connect these pathways/processes are keys to the future of research on human aging. An important component of mitochondrial health preservation is mitophagy, and this and other areas that are particularly ripe for future investigation will be discussed.

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“…17 It is capable of acetylating p53, thereby reducing the ability of p53 to induce apoptosis. 18 Calapre et al 19 showed that activation of SIRT1 could promote the acetylation of p53, thereby inhibiting apoptosis caused by DNA damage. Zheng T et al 20 found that SIRT1 was downregulated in LEC cells under oxidative stress and the ability of SIRT1 to inhibit p53-dependent apoptosis could protect LEC cells against oxidative stress.…”

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confidence: 99%

miR‐23b‐3p regulates apoptosis and autophagy via suppressing SIRT1 in lens epithelial cells

Zhou

Wang

et al. 2019

J of Cellular Biochemistry

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Age-related cataract is one of the prior causes of blindness and the incidence rates of cataract are even rising. Oxidative stress plays an important role in the pathogenesis of cataracts. Under oxidative stress, lens epithelial cell (LEC cell) apoptosis is activated, which might lead to the opacity of the lens and accelerate the progression of cataract development. Meanwhile, autophagy is also active to face oxidative stress. miRNAs have been reported to involve cataract. However, the underlying mechanism is not clear. The present study aimed to investigate the regulatory effect of miR23b-3p on apoptosis and autophagy in LEC cells under oxidative stress. The expression levels of miR-23b-3p were examined in age-related cataract tissues and LEC cells treated with hydrogen peroxide, showing that miR23b-3p expression levels were upregulated. Knockdown of miR23b-3p expression in LEC cells brought about apoptosis significantly decreased while autophagy significantly increased during hydrogen peroxide.We predicted microRNA miRNA-23b-3p might participate in regulating silent information regulator 1 (SIRT1) by bioinformatics database of TargetScan. Luciferase reporter assays confirmed that miRNA-23b-p could suppress SIRT1 expression by binding its 3′UTR. In addition, overexpression or knockdown of miR-23b-3p could decrease or increase SIRT1 expression, which indicated that Mir-23b-3p could suppress SIRT1 expression. In addition, enhanced SIRT1 could attenuate the regulation of cell apoptosis and autophagy induced by overexpression of miR-23b-3p. Taken together, our findings revealed that miR-23b-3p regulated apoptosis and autophagy via suppressing SIRT1 in LEC cell under oxidative stress, which could provide new ideas for clinical treatment of cataract. K E Y W O R D Sapoptosis, autophagy, cataract, miR-23b-p, SIRT1

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SIRT1 activation mediates heat-induced survival of UVB damaged Keratinocytes

Cited by 7 publications

References 59 publications

Sirtuin 1 and Skin: Implications in Intrinsic and Extrinsic Aging—A Systematic Review

Sirtuin 1 and Skin: Implications in Intrinsic and Extrinsic Aging—A Systematic Review

Toward understanding genomic instability, mitochondrial dysfunction and aging

miR‐23b‐3p regulates apoptosis and autophagy via suppressing SIRT1 in lens epithelial cells

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