2. Academic Validation
  3. Role of ROS-mediated PERK/ATF4 signaling activation in extracorporeal tube formation injury of human umbilical vein endothelial cells induced by cooking oil fume PM2.5 exposure

Role of ROS-mediated PERK/ATF4 signaling activation in extracorporeal tube formation injury of human umbilical vein endothelial cells induced by cooking oil fume PM2.5 exposure

  • Ecotoxicol Environ Saf. 2023 Sep 15:263:115332. doi: 10.1016/j.ecoenv.2023.115332.
Shu Sun 1,  Chao Zhang 2,  Qi Zhang 3,  Changlian Li 4,  Dan Huang 1,  Rui Ding 5,  Jiyu Cao 6,  Jiahu Hao 7
Affiliations

Affiliations

  • 1 Department of Maternal, Child and Adolescent Health, School of Public Health, Anhui Medical University, No 81 Meishan Road, Hefei 230032, Anhui, China.
  • 2 Teaching Center for Preventive Medicine, School of Public Health, Anhui Medical University, No 81 Meishan Road, Hefei 230032, Anhui, China.
  • 3 Hefei Institutes of Physical Science Chinese Academy of Sciences, No 350 Shushanhu Road, Hefei 230001, Anhui, China.
  • 4 Department of Environmental Health, Hefei Center for Disease Control and Prevention, No 86 Lu'an Road, Hefei 230061, Anhui, China.
  • 5 Department of Occupational Health and Environmental Health, School of Public Health, Anhui Medical University, No 81 Meishan Road, Hefei, Anhui, 230032, China.
  • 6 Teaching Center for Preventive Medicine, School of Public Health, Anhui Medical University, No 81 Meishan Road, Hefei 230032, Anhui, China. Electronic address: [email protected].
  • 7 Department of Maternal, Child and Adolescent Health, School of Public Health, Anhui Medical University, No 81 Meishan Road, Hefei 230032, Anhui, China. Electronic address: [email protected].
PMID: 37611476 DOI: 10.1016/j.ecoenv.2023.115332
Abstract

Cooking oil fume-derived PM2.5 (COF-PM2.5) is a major source of indoor air contamination in China, which has been demonstrated to be a hazard factor of cardiovascular and cerebrovascular diseases. This study aimed to investigate the role of ROS-mediated PERK/ATF4 signaling activation in COF-PM2.5-inhibited extracorporeal tube formation in human umbilical vein endothelial cells (HUVECs). HUVECs were treated with 100 μg/mL COF-PM2.5 at different times, with or without 100 nM PERK activity inhibitor GSK2606414 (GSK) or 200 μM antioxidant N-acetylcysteine (NAC) pretreatment. Our results showed that COF-PM2.5 exposure can inhibit extracorporeal tube formation and down-regulate VEGFR2 expression in HUVECs. Furthermore, our data indicated that COF-PM2.5 exposure can activate the PERK/ATF4 signaling in HUVECs. Mechanistically, pretreatment with GSK interdicted PERK/ATF4 signaling, thereby reversing COF-PM2.5-downregulated VEGFR2 protein expression in HUVECs. Furthermore, NAC reversed VEGFR2 expression downregulated induced by COF-PM2.5 by inhibiting the upregulation of intracellular ROS levels and PERK/ATF4 signaling in HUVECs. As above, COF-PM2.5 exposure could induce ROS release from HUVECs, which in turn activate the endoplasmic reticulum PERK/ATF4 signaling and inhibit tube formation of HUVECs.

Keywords

Cooking oil fume; PERK; PM(2.5); Tube formation.

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