Antioxidants prevent particulate matter-induced senescence of lung fibroblasts

被引:4
作者
Jin, Sein [1 ,2 ]
Yoon, Sung-Jin [3 ]
Jung, Na-Young
Lee, Wang Sik
Jeong, Jinyoung [3 ,4 ,5 ]
Park, Young-Jun
Kim, Wantae [2 ]
Oh, Doo-Byoung [1 ,4 ]
Seo, Jinho [1 ,4 ]
机构
[1] Korea Res Inst Biosci & Biotechnol KRIBB, Aging Convergence Res Ctr, Daejeon 34141, South Korea
[2] Chungnam Natl Univ, Dept Biochem, Daejeon 34134, South Korea
[3] KRIBB, Environm Dis Res Ctr, Daejeon 34141, South Korea
[4] Univ Sci & Technol UST, KRIBB Sch Biotechnol, Dept Biosyst & Bioengn, Daejeon 34113, South Korea
[5] UST, KRIBB Sch Biosci, Dept Biomol Sci, Daejeon 34113, South Korea
关键词
Particulate matter; Cellular senescence; Reactive oxygen species; DNA damage Response; Antioxidants; CELLULAR SENESCENCE; DNA-DAMAGE; OXIDATIVE STRESS; ROS GENERATION; PM10; EXPOSURE; CELLS; ACTIVATION; CANCER; MECHANISMS; INHIBITORS;
D O I
10.1016/j.heliyon.2023.e14179
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Particulate matter (PM) contributes to human diseases, particularly lung disease; however, the molecular mechanism of its action is yet to be determined. Herein, we found that prolonged PM exposure induced the cellular senescence of normal lung fibroblasts via a DNA damage-mediated response. This PM-induced senescence (PM-IS) was only observed in lung fibroblasts but not in A549 lung adenocarcinoma cells. Mechanistic analysis revealed that reactive oxygen species (ROS) activate the DNA damage response signaling axis, increasing p53 phosphorylation, ultimately leading to cellular senescence via an increase in p21 expression without affecting the p16pRB pathway. A549 cells, instead, were resistant to PM-IS due to the PM-induced ROS production suppression. Water-soluble antioxidants, such as vitamin C and N-Acetyl Cysteine, were found to alleviate PM-IS by suppressing ROS production, implying that antioxidants are a promising therapeutic intervention for PM-mediated lung pathogenesis.
引用
收藏
页数:16
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