Selenium Suppresses Lipopolysaccharide-Induced Fibrosis in Peritoneal Mesothelial Cells Through Inhibition of Epithelial-to-Mesenchymal Transition

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• 作者：Jinyan Liu (1)
  Lingling Zeng (2)
  Yuliang Zhao (3)
  Bin Zhu (4)
  Wanjun Ren (4)
  Chunling Wu (4)
  
• 关键词：Lipopolysaccharides ; Epithelial ; to ; mesenchymal transition ; Selenium ; Reactive oxygen species ; PI3K/AKT
• 刊名：Biological Trace Element Research
• 出版年：2014
• 出版时间：November 2014
• 年：2014
• 卷：161
• 期：2
• 页码：202-209
• 全文大小：1,264 KB
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• 作者单位：Jinyan Liu (1)
  Lingling Zeng (2)
  Yuliang Zhao (3)
  Bin Zhu (4)
  Wanjun Ren (4)
  Chunling Wu (4)
  
  1. Department of Nephrology, Jining No.1 People’s Hospital, Jining, 272100, Shandong, People’s Republic of China
  2. Department of Nephrology, Xinhua hospital of Chengdu, Chengdu, 610066, Sichuan, People’s Republic of China
  3. Department of Nephrology, West China Hospital, West China School of Medicine, Sichuan University, Sichuan, 610041, People’s Republic of China
  4. Department of Nephrology and Hemodialysis, Jinan Central Hospital, Shandong University, No. 105, Jiefang Road, Jinan, 250013, Shandong, People’s Republic of China
  
• ISSN：1559-0720

文摘

Peritoneal fibrosis resulting from long-term clinical peritoneal dialysis has been the main reason of dropout from peritoneal dialysis. Peritonitis as a common complication of peritoneal dialysis treatment may lead to the occurrences of peritoneal fibrosis. We cultured peritoneal mesothelial cells with lipopolysaccharides (LPS) in order to stimulate the environment of peritonitis and investigate whether lipopolysaccharides could induce epithelial-to-mesenchymal transition (EMT). Oxidative stress could stimulate fibrogenesis while selenium has antioxidant properties. So, this study also explored whether selenium supplementation affects lipopolysaccharide-induced EMT and fibrosis. We found that lipopolysaccharides could activate EMT changes such as the loss of E-cadherin and the increase of α-smooth muscle actin (α-SMA), collagen I, vimentin, and fibronectin (FN), while selenium inhibits EMT by modulating reactive oxygen species (ROS) generation and ROS/MMP-9 signaling pathways in peritoneal mesothelial cells. Moreover, it was revealed that selenium decreased the EMT events of peritoneal mesothelial cells via inhibition of PI3k/AKT pathways. In conclusion, these findings enable a better understanding of the mechanism of peritoneal fibrosis and explore a new idea for the prevention and treatment.