ArticleEnvironmental health perspectives2014
Acrolein-exposed normal human lung fibroblasts in vitro: cellular senescence, enhanced telomere erosion, and degradation of Werner's syndrome protein.
Article in Environmental health perspectives, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Assessment of cellular senescence potential of PM2.5 using 3D human lung fibroblast spheroids in vitro model.Toxicology research · 2024Article
- The Peroxidation of Lipids, Cellular Senescence and Aging.Journal of aging science · 2024Article
- [Effects of Acrolein on the Proliferation of andSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021Article
- Senescence in Pulmonary Fibrosis: Between Aging and Exposure.Frontiers in medicine · 2020Review
- A Novel Compound, "FA-1" Isolated from Prunus mume, Protects Human Bronchial Epithelial Cells and Keratinocytes from Cigarette Smoke Extract-Induced Damage.Scientific reports · 2018Article
- Article
- APO-9'-Fucoxanthinone Extracted from Undariopsis peteseniana Protects Oxidative Stress-Mediated Apoptosis in Cigarette Smoke-Exposed Human Airway Epithelial Cells.Marine drugs · 2016Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundAcrolein is a ubiquitous environmental hazard to human health. Acrolein has been reported to activate the DNA damage response and induce apoptosis. However, little is known about the effects of acrolein on cellular senescence.
objectivesWe examined whether acrolein induces cellular senescence in cultured normal human lung fibroblasts (NHLF).
methodsWe cultured NHLF in the presence or absence of acrolein and determined the effects of acrolein on cell proliferative capacity, senescence-associated β-galactosidase activity, the known senescence-inducing pathways (e.g., p53, p21), and telomere length.
resultsWe found that acrolein induced cellular senescence by increasing both p53 and p21. The knockdown of p53 mediated by small interfering RNA (siRNA) attenuated acrolein-induced cellular senescence. Acrolein decreased Werner's syndrome protein (WRN), a member of the RecQ helicase family involved in DNA repair and telomere maintenance. Acrolein-induced down-regulation of WRN protein was rescued by p53 knockdown or proteasome inhibition. Finally, we found that acrolein accelerated p53-mediated telomere shortening.
conclusionsThese results suggest that acrolein induces p53-mediated cellular senescence accompanied by enhanced telomere attrition and WRN protein down-regulation.
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