2. Academic Validation
  3. Acrolein induces NLRP3 inflammasome-mediated pyroptosis and suppresses migration via ROS-dependent autophagy in vascular endothelial cells

Acrolein induces NLRP3 inflammasome-mediated pyroptosis and suppresses migration via ROS-dependent autophagy in vascular endothelial cells

  • Toxicology. 2018 Dec 1;410:26-40. doi: 10.1016/j.tox.2018.09.002.
Chunteng Jiang 1,  Liping Jiang 2,  Qiannan Li 3,  Xiaofang Liu 4,  Tianjiao Zhang 1,  Linlin Dong 1,  Tiehong Liu 1,  Li Liu 1,  Guoling Hu 1,  Xiance Sun 5,  Lijie Jiang 6
Affiliations

Affiliations

  • 1 Department of Internal Medicine, The Affiliated Zhong Shan Hospital of Dalian University, Dalian, 116001, Liaoning, PR China.
  • 2 Preventive Medicine Laboratory, College of Public Health, Dalian Medical University, No. 9, West Segment of South lvshun Road, Dalian, 116044, Liaoning, PR China; Natural Products Engineering Technology Center, Dalian Medical University, No. 9, West Segment of South lvshun Road, Dalian, 116044, Liaoning, PR China.
  • 3 Department of Data Analytics, Street Easy Company, 130 5th Ave, New York, 10011, USA.
  • 4 Natural Products Engineering Technology Center, Dalian Medical University, No. 9, West Segment of South lvshun Road, Dalian, 116044, Liaoning, PR China; Department of Nutrition and Food Safety, College of Public Health, Dalian Medical University, No. 9, West Segment of South lvshun Road, Dalian, 116044, Liaoning, PR China.
  • 5 Natural Products Engineering Technology Center, Dalian Medical University, No. 9, West Segment of South lvshun Road, Dalian, 116044, Liaoning, PR China; Department of Occupational and Environmental Health, College of Public Health, Dalian Medical University. No. 9, West Segment of South lvshun Road, Dalian, 116044, Liaoning, PR China.
  • 6 Department of Internal Medicine, The Affiliated Zhong Shan Hospital of Dalian University, Dalian, 116001, Liaoning, PR China. Electronic address: jianglijie1227@126.com.
PMID: 30205151 DOI: 10.1016/j.tox.2018.09.002
Abstract

Acrolein is a common environmental pollutant that has been linked to cardiovascular diseases, such as atherosclerosis (AS). Increasing evidence demonstrates that acrolein impairs the cardiovascular system by targeting vascular endothelial cells, but the underlying mechanisms haven't been completely elucidated. In human umbilical vein endothelial cells (HUVECs), we observed that acrolein treatment induced cell Reactive Oxygen Species (ROS) generation, Autophagy, Pyroptosis and reduced cell migration. In addition, exposure to acrolein resulted in NLRP3 inflammasome activation as evidenced by cleavage of Caspase-1 and downstream mature interleukin (IL)-1β and IL-18 secretion. Knockdown of NLRP3 by small interfering RNA remarkably suppressed acrolein-induced Pyroptosis and increased cell migration. Moreover, the scavenging ROS relieved the Autophagy, NLRP3 inflammasome activation and Pyroptosis. Furthermore, the role of Autophagy in the acrolein-medicated Pyroptosis and cell migration was investigated. In our study, 3-methyladenine (3-MA), an Autophagy Inhibitor, aggravated NLRP3 inflammasome activation, Pyroptosis and decreased cell migration, rapamycin (Rapa), an Autophagy inducer, alleviated aforementioned phenomenon under acrolein stress. Besides, we found damaged mitochondrion accentuated NLRP3 inflammasome and Pyroptosis in acrolein-treated cells. In conclusion, it is possible that acrolein induced cell Pyroptosis and suppressed cell migration via ROS-dependent Autophagy. What's more, NLRP3 inflammasome activation plays a key role in this process.

Keywords

Acrolein; Autophagy; Migration; NLRP3 inflammasome; Pyroptosis; ROS.

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