Polycomb group proteins: Novel molecules associated with ultraviolet A-induced photoaging of human skin

Wu, Zhuoxia; Zhang, Lianbo

doi:10.3892/etm.2017.4807

Cited by 9 publications

(6 citation statements)

References 55 publications

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“…These findings provide evidence that Bmi-1 plays a protective role against intrinsic skin aging. Consist with previous studies [14,23], in our study, we confirmed that hair follicles, keratinocytes, and fibroblasts have relatively stronger expression levels of Bmi-1 localization. Long considered both physiologic and inevitable, skin aging is a degenerative phenomenon progressively with age [24].…”

Section: Discussionsupporting

confidence: 91%

Repression of the Antioxidant Pyrroloquinoline Quinone in Skin Aging Induced by Bmi-1 Deficiency

Liu

Liang

et al. 2022

BioMed Research International

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It is uncertain whether Bmi-1 deficiency could lead to skin aging by redox imbalance and DNA damage. In this study, we first confirmed that Bmi-1 had a relatively high expression level in the skin and Bmi-1 expression levels gradually decreased with age. Then, we studied the role of Bmi-1 in the skin using a Bmi-1-/- mouse model. Bmi-1-/- mice were supplemented with or without pyrroloquinoline quinone (PQQ) for 5 weeks, and their skin phenotypes were compared with Bmi1-/- and wild-type littermates. Our results showed that Bmi-1-/- mice displayed decreased vertical thickness of skin, sparse hair follicles, and thinner and more irregular collagen bundles. Mechanistically, increased oxidative stress with reducing antioxidant capacity and induced DNA damage occurred in Bmi-1-/- mice. Subsequently, this would lead to reduced cell proliferation, increased cell senescence and matrix metalloproteinases (MMPs), and the degradation of fibroblast function and further reduce collagen synthesis. All pathological alterations in the skin of Bmi-1-/- mice were alleviated by PQQ supplementation. These results demonstrated that Bmi-1 might play a key role in protection from skin aging by maintaining redox balance and inhibiting DNA damage response and will be a novel and potential target for preventing skin aging.

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Section: Discussionsupporting

confidence: 91%

Repression of the Antioxidant Pyrroloquinoline Quinone in Skin Aging Induced by Bmi-1 Deficiency

Liu

Liang

et al. 2022

BioMed Research International

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“…All samples were analyzed in duplicate, and the results are presented as relative gene expression using the ΔΔct method. HPRT1 , HMBS , and RPL13A primer sequences were based on the work of Vandesompele et al [ 17 ], while other primers were based on sequences published elsewhere: CD44s [ 18 ], RHAMM [ 19 ], ICAM-1 [ 20 ], LYVE-1 [ 21 ], TLR4 [ 22 ], HYAL1 , HYAL2 [ 23 ], and HYAL3 [ 24 ]. Other sequences were designed using Primer3 software [ 25 ] or PrimerBlast [ 26 ].…”

Section: Methodsmentioning

confidence: 99%

Hypoxia modulates human mast cell adhesion to hyaluronic acid

et al. 2021

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Hypoxia is an inherent factor in the inflammatory process and is important in the regulation of some immune cell functions, including the expression of mast cell pro- and anti-inflammatory mediators. Hypoxia also influences cell adhesion to the extracellular matrix (ECM). Hyaluronic acid is one of the major components of the ECM that is involved in inflammatory and tissue regeneration processes in which mast cells play a prominent role. This prompted us to investigate the effects of hypoxia on the expression of hyaluronic acid receptors in mast cells and mast cell adhesion to this ECM component. We found that human LAD2 mast cells spontaneously adhered to hyaluronic acid in a CD44-dependent manner and that reduced oxygen concentrations inhibited or even completely abolished this adhesion process. The mechanism of hypoxia downregulation of mast cell adhesion to hyaluronic acid did not involve a decrease in CD44 expression and hyaluronidase-mediated degradation of adhesion substrates but rather conformational changes in the avidity of CD44 to hyaluronic acid. Hypoxia-mediated regulation of mast cell adhesion to extracellular matrix components might be involved in the pathogenic accumulation of mast cells observed in the course of certain diseases including rheumatoid arthritis and cancer.

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“…Indeed, UV-A radiations modulate the expression of EZH2 and Bmi-1 , induce the senescence of human dermal fibroblasts and reduce hyaluronic acid (HA) synthesis. The use of GSK126, an inhibitor of the EZH2-methyl transferase activity, restores dermal fibroblasts growth after UV-A irradiation by modulating the expression of enzymes involved in HA synthesis and inhibiting the transcription of various photo-aging-related genes (e.g., Smad2 , Smad4 , MMP-1 ) [102,103]. Moreover, UV-B radiations induce human dermal fibroblast senescence through miR-101 induction and EZH2 reduction [104].…”

Section: Epigenetic Changes In Skin Agingmentioning

confidence: 99%

Epigenetic Regulation of Skin Cells in Natural Aging and Premature Aging Diseases

Orioli

Dellambra

2018

Cells

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Skin undergoes continuous renewal throughout an individual’s lifetime relying on stem cell functionality. However, a decline of the skin regenerative potential occurs with age. The accumulation of senescent cells over time probably reduces tissue regeneration and contributes to skin aging. Keratinocytes and dermal fibroblasts undergo senescence in response to several intrinsic or extrinsic stresses, including telomere shortening, overproduction of reactive oxygen species, diet, and sunlight exposure. Epigenetic mechanisms directly regulate skin homeostasis and regeneration, but they also mark cell senescence and the natural and pathological aging processes. Progeroid syndromes represent a group of clinical and genetically heterogeneous pathologies characterized by the accelerated aging of various tissues and organs, including skin. Skin cells from progeroid patients display molecular hallmarks that mimic those associated with naturally occurring aging. Thus, investigations on progeroid syndromes strongly contribute to disclose the causal mechanisms that underlie the aging process. In the present review, we discuss the role of epigenetic pathways in skin cell regulation during physiologic and premature aging.

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Polycomb group proteins: Novel molecules associated with ultraviolet A-induced photoaging of human skin

Cited by 9 publications

References 55 publications

Repression of the Antioxidant Pyrroloquinoline Quinone in Skin Aging Induced by Bmi-1 Deficiency

Repression of the Antioxidant Pyrroloquinoline Quinone in Skin Aging Induced by Bmi-1 Deficiency

Hypoxia modulates human mast cell adhesion to hyaluronic acid

Epigenetic Regulation of Skin Cells in Natural Aging and Premature Aging Diseases

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