Research Advance Publication
Acrolein-Exposed Normal Human Lung Fibroblasts in Vitro: Cellular Senescence, Enhanced Telomere Erosion, and Degradation of Werner’s Syndrome Protein
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Citation: Jang JH, Bruse S, Huneidi S, Schrader RM, Monick MM, Lin Y, Carter AB, Klingelhutz AJ, Nyunoya T. Acrolein-Exposed Normal Human Lung Fibroblasts in Vitro: Cellular Senescence, Enhanced Telomere Erosion, and Degradation of Werner’s Syndrome Protein. Environ Health Perspect; http://dx.doi.org/10.1289/ehp.1306911.
Received: 8 April 2013
Accepted: 15 April 2014
Advance Publication: 18 April 2014
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Background: Acrolein is a carcinogenic and ubiquitous environmental hazard to human health. Acrolein activates the DNA damage response and induces apoptosis. However, little is known about the effects of acrolein on cellular senescence.
Objectives: In this study, we investigated whether acrolein induces cellular senescence in cultured normal human lung fibroblasts (NHLF).
Methods: We 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.
Results: We found that acrolein induced cellular senescence by increasing both p53 and p21. siRNA-mediated knockdown of p53 attenuated acrolein-induced cellular senescence. Acrolein decreased Werner’s syndrome protein (WRN protein), a member of the RecQ helicase family involved in DNA repair and telomere maintenance. Acrolein-induced downregulation of WRN protein was rescued by p53 knockdown or proteasome inhibition. Finally, we found that acrolein accelerates p53-mediated telomere shortening.
Conclusions: These results suggest that acrolein induces p53-mediated cellular senescence accompanied by enhanced telomere attrition and WRN protein downregulation.
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