Changes in Zn homeostasis during long term culture of primary endothelial cells and effects of Zn on endothelial cell senescence
Open accessAbstract
Endothelial cell senescence and Zn nutritional status influence cardiovascular disease. The influence of Zn appears dichotomous, hence it is imperative to understand the relationship with cellular senescence to improve knowledge about the molecular and cellular basis of the disease. Here we aimed to determine: 1) the impact of chronic exposure to a moderately high dose of Zn on senescence of endothelial cells; 2) the changes in Zn homeostasis during the lifespan of primary cultured endothelial cells; and 3) the susceptibility of proliferating and senescent endothelial cells to cell death after short term exposure to increasing doses of Zn and of the Zn chelator TPEN. Chronic exposure to Zn accelerated senescence and untreated cells at later passages, where doubling time had increased, displayed relocation of labile Zn and altered expression of genes involved in the response to Zn toxicity, including SLC30A1, SLC39A6, SLC30A5, SLC30A10 and metallothioneins, indicating that senescent cells have altered zinc homeostasis. Most Zn-dependent genes that were expressed differently between early and late passages were correlated with changes in the expression of anti-apoptotic genes. Short-term treatment with a high dose of Zn leads to cell death, but only in the population of cells at both earlier and later passages that had already entered senescence. In contrast, Zn depletion led to death of cells at earlier but not later passages, which suggests that there are sub-populations of senescent cells that are resistant to Zn depletion. This resistant senescent cell population may accumulate under conditions of Zn deficiency and contribute to vascular pathology.
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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 [411]
Zinc overload can contribute to increased cellular oxidative stress and senescence through mechanisms possibly related to organelle dysfunction.
“On the other hand, Zn overload can contribute to augment cellular OS and senescence through different mechanisms not yet well-defined, but possibly related to organelles dysfunction [411,427,438].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [411]
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- Authors
- Malavolta, M., Costarelli, L., Giacconi, R., Basso, A., Piacenza, F., Pierpaoli, E., Provinciali, M., Ogo, O. A., & Ford, D.
- Affiliations
- Istituto Nazionale di Riposo e Cura per Anziani (IT)
- Newcastle University (GB)
- Northumbria University (GB)
- Corresponding author
- Malavolta, Marco
- ORCID
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2017-12
- Volume
- 99
- Pages
- 35-45
- ISSN
- 0531-5565 (ISSN-L)
- OpenAlex
- W2754293248
- Cited by
- 37
- References
- 47
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 7 · 2022: 3 · 2021: 4 · 2020: 4 · 2018: 9 · 2017: 1
- FWCI
- 3.18
- Type
- journal article
- Language
- en
- Open access
- Locations
- Experimental Gerontology (publishedVersion)
- PubMed (publishedVersion)
- Northumbria Research Link (Northumbria University) (submittedVersion)
- Università Politecnica delle Marche (Università Politecnica delle Marche) (submittedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- FA (TD1304)
- UK Biotechnology and Biological Sciences Research Council (BB/F019637/1)
- Benue State University
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
- Keywords
- zinc homeostasis, endothelial cell senescence, zinc toxicity, TPEN, labile zinc, metallothionein, zinc transporters, SLC39A6, SLC30A10, apoptosis, zinc deficiency, zinc depletion, cardiovascular disease, primary endothelial cells
- MeSH terms
- Cells, Cultured, Chelating Agents, Dose-Response Relationship, Drug, Ethylenediamines, Gene Expression Regulation, Homeostasis, Humans, Time Factors, Cellular Senescence, Apoptosis, Zinc Sulfate, Gene Expression Profiling, Databases, Genetic, Endothelial Cells, Cell Shape, Cell Proliferation, Primary Cell Culture, Human Umbilical Vein Endothelial Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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