Ammonia inhalation-mediated mir-202-5p leads to cardiac autophagy through PTEN/AKT/mTOR pathway

被引:71
|
作者
Xing, Houjuan [1 ]
Peng, Muqiao [1 ]
Li, Zhuo [1 ]
Chen, Jianqing [1 ]
Zhang, Hongfu [2 ]
Teng, Xiaohua [1 ]
机构
[1] Northeast Agr Univ, Coll Anim Sci & Technol, Harbin 150030, Heilongjiang, Peoples R China
[2] Chinese Acad Agr Sci, Inst Anim Sci, State Key Lab Anim Nutr, Beijing 100193, Peoples R China
关键词
Environmental contaminant; Ammonia; PTEN/AKT/mTOR pathway; Heart injury; Risk assessment; INDUCED OXIDATIVE STRESS; SIGNALING PATHWAY; INDUCED APOPTOSIS; AKT/MTOR PATHWAY; HYDROGEN-SULFIDE; EXPRESSION; TOXICITY; EXPOSURE; ACTIVATION; EMISSIONS;
D O I
10.1016/j.chemosphere.2019.06.235
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Ammonia is a known environmental pollutant around the world. It leads to the deterioration of air quality and has adverse effects on human health. Although previous studies have demonstrated that ammonia caused some health problems to chickens, it is still unclear whether ammonia causes cardiac toxicity. The functional autophagy is very important for cardiac homeostasis. Therefore, the role of autophagy was investigated in the mechanism of chicken heart damage induced by environmental contaminant ammonia in our present study. The results from the oxidative stress index (SOD, GPx, H2O2, and MDA), NO content, iNOS activity, and transmission electron microscopy indicated that excess ammonia induced oxidative stress and autophagy in the chicken heart. The expression results from miR-202-5p and PTEN/AKT/mTOR (PTEN, LC3-I, LC3-II, p-AKT, AKT, Beclin1, Dynein, ATG5, p-mTOR and mTOR) signaling pathway-related genes further confirmed that excess ammonia induced cardiac autophagy. In conclusion, these results demonstrated that excess ammonia can cause cardiac damage and mediate mir-202-5p to regulate autophagy through PTEN/AKT/mTOR pathway in the chicken heart injury. Our findings will provide a new insight for better assessing the toxicity mechanism of environmental pollutants ammonia on the heart. (C) 2019 Elsevier Ltd. All rights reserved.
引用
收藏
页码:858 / 866
页数:9
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