Skin melanocytes and fibroblasts show different changes in choline metabolism during cellular senescence

Windler, Cordula; Gey, Claudia; Seeger, Karsten

doi:10.1016/j.mad.2017.05.001

Cited by 11 publications

(12 citation statements)

References 50 publications

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“…Regarding ageing, only two metabolic studies on epidermis samples 45 and cell models 46 were identified. The effects of various xenobiotics have been investigated in seven studies and an additional study of co‐exposure to UV/B[a]P by Yang et al (2021) 61 .…”

Section: Resultsmentioning

confidence: 99%

“…109 In ageing, the described alterations in metabolites involved in the methionine-glutathione metabolism pointed to similar regulations as in sun-exposed skin (Figure 2). 46,81 Metabolites involved in cysteine metabolism were also elevated in PSen cells. 65 Polycyclic aromatic hydrocarbon exposure lowered levels of precursors of the GSH, which was interpreted by the authors as a sign towards enhanced biosynthesis.…”

Section: Methionine-glutathione Metabolismmentioning

confidence: 97%

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A systematic review: metabolomics‐based identification of altered metabolites and pathways in the skin caused by internal and external factors

Masutin

Kersch

Schmitz‐Spanke

2022

Experimental Dermatology

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The skin's ability to function optimally is affected by many diverse factors. Metabolomics has a great potential to improve our understanding of the underlying metabolic changes and the affected pathways. Therefore, the objective of this study was to review the current state of the literature and to perform further metabolic pathway analysis on the obtained data. The aim was to gain an overview of the metabolic changes under altered conditions and to identify common and different patterns as a function of the investigated factors. A cross‐study comparison of the extracted studies from different databases identified 364 metabolites, whose concentrations were considerably altered by the following factor groups: irradiation, xenobiotics, ageing and skin diseases (mainly psoriasis). Using metabolic databases and pathway analysis tools, the individual metabolites were assigned to the corresponding metabolic pathways and the most strongly affected signalling pathways were identified. All factors induced oxidative stress. Thus, antioxidant defence systems, especially coenzyme Q10 (ageing) and the glutathione system (irradiation, ageing, xenobiotics), were impacted. Lipid metabolism was also impacted by all factors studied. The carnitine shuttle as part of β‐oxidation was activated by all factor groups except ageing. Glycolysis, Krebs (TCA) cycle and purine metabolism were mainly affected by irradiation and xenobiotics. The pentose phosphate pathway was activated, and Krebs cycle was downregulated in response to oxidative stress. In summary, it can be ascertained that mainly energy metabolism, lipid metabolism, antioxidative defence and DNA repair systems were impacted by the factors studied.

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Section: Resultsmentioning

confidence: 99%

Section: Methionine-glutathione Metabolismmentioning

confidence: 97%

A systematic review: metabolomics‐based identification of altered metabolites and pathways in the skin caused by internal and external factors

Masutin

Kersch

Schmitz‐Spanke

2022

Experimental Dermatology

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“…We also noted the induction of p27, another senescence marker, in the oncogenic melanocytes ( Figure S1A ). We also observed the formation of senescence-associated heterochromatin foci (SAHF), a distinct chromatin organization found in senescent cells [ 26 ], as evidenced by the punctate staining of the nuclei in the BRAF V600E -transformed melanocytes ( Figure S1B ). These results demonstrated that the BRAF V600E oncogene induced OIS and growth arrest in human primary melanocytes.…”

Section: Resultsmentioning

confidence: 93%

Role of the Skin Microenvironment in Melanomagenesis: Epidermal Keratinocytes and Dermal Fibroblasts Promote BRAF Oncogene-Induced Senescence Escape in Melanocytes

Sadangi

Milosavljevic

Castro‐Pérez

et al. 2022

Cancers

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BRAFV600E is the most common mutation driver in melanoma. This mutation is known to cause a brief burst of proliferation followed by growth arrest and senescence, which prevent an uncontrolled cell proliferation. This phenomenon is known as oncogene-induced senescence (OIS) and OIS escape is thought to lead to melanomagenesis. Much attention has been focused on the melanocyte-intrinsic mechanisms that contribute to senescence escape. Additional genetic events such as the loss of tumor suppressor PTEN and/or epigenetic changes that contribute to senescence escape have been described. However, the role of the skin microenvironment—specifically, the role of epidermal keratinocytes—on melanomagenesis is not fully understood. In this study, we employ a microfluidic platform to study the interaction between melanocytes expressing the BRAFV600E mutation as well as keratinocytes and dermal fibroblasts. We demonstrate that keratinocytes suppress senescence-related genes and promote the proliferation of transformed melanocytes. We also show that a keratinocyte-conditioned medium can alter the secretion of both pro- and anti-tumorigenic factors by transformed melanocytes. In addition, we show that melanocytes and keratinocytes from donors of white European and black African ancestry display different crosstalks; i.e., white keratinocytes appear to promote a more pro-tumorigenic phenotype compared with black keratinocytes. These data suggest that keratinocytes exert their influence on melanomagenesis both by suppressing senescence-related genes in melanocytes and by affecting the balance of the melanocyte-secreted factors that favor tumorigenesis.

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“…This is in agreement with the dynamic nature of the continually renewing epidermis. Nevertheless, senescence was shown to differentially influence choline metabolism in fibroblasts and melanocytes [ 216 ]. Senescent human skin fibroblasts showed elevated levels of glycerol-phosphocholine (GPC).…”

Section: Cellular Senescence In Skin Agingmentioning

confidence: 99%

Skin Aging, Cellular Senescence and Natural Polyphenols

Csekes

Račková

2021

IJMS

147

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The skin, being the barrier organ of the body, is constitutively exposed to various stimuli impacting its morphology and function. Senescent cells have been found to accumulate with age and may contribute to age-related skin changes and pathologies. Natural polyphenols exert many health benefits, including ameliorative effects on skin aging. By affecting molecular pathways of senescence, polyphenols are able to prevent or delay the senescence formation and, consequently, avoid or ameliorate aging and age-associated pathologies of the skin. This review aims to provide an overview of the current state of knowledge in skin aging and cellular senescence, and to summarize the recent in vitro studies related to the anti-senescent mechanisms of natural polyphenols carried out on keratinocytes, melanocytes and fibroblasts. Aged skin in the context of the COVID-19 pandemic will be also discussed.

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Skin melanocytes and fibroblasts show different changes in choline metabolism during cellular senescence

Cited by 11 publications

References 50 publications

A systematic review: metabolomics‐based identification of altered metabolites and pathways in the skin caused by internal and external factors

A systematic review: metabolomics‐based identification of altered metabolites and pathways in the skin caused by internal and external factors

Role of the Skin Microenvironment in Melanomagenesis: Epidermal Keratinocytes and Dermal Fibroblasts Promote BRAF Oncogene-Induced Senescence Escape in Melanocytes

Skin Aging, Cellular Senescence and Natural Polyphenols

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