Interplay between Selenium Levels, Selenoprotein Expression, and Replicative Senescence in WI-38 Human Fibroblasts
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Selenium is an essential trace element, which is incorporated as selenocysteine into at least 25 selenoproteins using a unique translational UGA-recoding mechanism. Selenoproteins are important enzymes involved in antioxidant defense, redox homeostasis, and redox signaling pathways. Selenium levels decline during aging, and its deficiency is associated with a marked increase in mortality for people over 60 years of age. Here, we investigate the relationship between selenium levels in the culture medium, selenoprotein expression, and replicative life span of human embryonic lung fibroblast WI-38 cells. Selenium levels regulate the entry into replicative senescence and modify the cellular markers characteristic for senescent cells. Whereas selenium supplementation extends the number of population doublings, its deficiency impairs the proliferative capacity of WI-38 cells. We observe that the expression of several selenoproteins involved in antioxidant defense is specifically affected in response to cellular senescence. Their expression is selectively controlled by the modulation of mRNA levels and translational recoding efficiencies. Our data provide novel mechanistic insights into how selenium impacts the replicative life span of mammalian cells by identifying several selenoproteins as new targets of senescence.
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The structural and functional roles of zinc, selenium, magnesium, copper, and manganese are crucial for antioxidant defence.
“Concerning the latter, the structural and functional roles of a few minerals such as zinc (Zn), selenium (Se), magnesium (Mg) copper (Cu) and manganese (Mn) is crucial (Table 5) [409,410,411,412,413,414,415,416,417,418,419,420].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [412]
In vitro, selenium supplementation reduces ROS levels, DNA damage, telomere shortening, and senescence biomarkers in bone marrow stromal cells, cultured human fibroblasts, and keratinocytes.
“For instance, in bone marrow stromal cells [443], cultured human fibroblasts [412], and keratinocytes [413], Se supplementation reduces ROS levels, DNA damage, telomere shortening and senescence biomarkers.”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [412]
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References 38 · Cited by 67
- Authors
- Legrain, Y., Touat-Hamici, Z., & Chavatte, L.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Chavatte, Laurent
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2014-02
- Volume
- 289
- Issue
- 9
- Pages
- 6299-6310
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC3937696
- OpenAlex
- W1979500586
- Cited by
- 67
- References
- 38
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 1 · 2023: 3 · 2022: 7 · 2021: 3 · 2020: 1 · 2019: 9 · 2018: 13 · 2017: 11 · 2016: 7 · 2015: 2 · 2014: 2
- FWCI
- 6.83
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Agence Nationale de la Recherche (ANR-09-BLAN-0048)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Selenium in Biological Systems
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Organoselenium and organotellurium chemistry
- Keywords
- selenium, selenoproteins, replicative senescence, WI-38 fibroblasts, replicative lifespan, selenocysteine, selenium deficiency, selenium supplementation, antioxidant defense, redox homeostasis, mRNA levels, cellular aging
- MeSH terms
- Animals, Cell Line, Fibroblasts, Gene Expression Regulation, Humans, RNA, Messenger, Selenium, Cellular Senescence, Cell Proliferation, Selenoproteins
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