Molecular mechanisms of melatonin in the reversal of LPS-induced EMT in peritoneal mesothelial cells

作者：Shi, Shuaishuai; Zhang, Yiqiang; Wen, Wenbin; Zhao, Yine; Sun, Lin^*

来源：Molecular Medicine Reports, 2016, 14(5): 4342-4348.

DOI：10.3892/mmr.2016.5744

• epithelial-mesenchymal transition
• lipopolysaccharide
• melatonin
• Toll-like receptor 4

Peritoneal dialysis (PD)-associated peritoneal fibrosis is a serious complication in patients with chronic renal failure on dialysis maintenance. Studies have shown that patients on long-term PD have chronic inflammation. The epithelial-to-mesenchymal transition (EMT) induced by inflammation is a major cause of peritoneal fibrosis and dysfunction. As a potent antioxidant property, melatonin has an antifibrotic effect. The present study investigated the effects of melatonin on lipopolysaccharide (LPS)-induced EMT and examined the molecular mechanisms in peritoneal mesothelial cells using western blotting, reverse transcription-polymerase chain reaction and immunofluorescence staining. The results of the study found that melatonin inhibited LPS-induced morphological changes, decreased the expression of LPS-induced markers of EMT, including vimentin and alpha-smooth muscle actin, and increased the expression of E-cadherin. In addition, it was found that the action of melatonin was mediated through the inactivation of the Toll-like receptor (TLR)4/c-Jun N-terminal kinase and TLR4/nuclear factor-kappa B-Snail signaling pathways. Thus, these data provided novel insight into the mechanisms underlying the function of melatonin in peritoneal mesothelial cells during the processes of EMT, and may provide a theoretical basis for the treatment of peritoneal fibrosis.

• 出版日期2016-11
• 单位中南大学; 长治医学院