UA promotes epithelial‑mesenchymal transition in peritoneal mesothelial cells

• Published in: Molecular medicine reports Vol. 20; no. 3; pp. 2396 - 2402
• Main Authors: Duan, Chao-Yang, Han, Jin, Zhang, Chong-Yu, Wu, Kunyi, Lin, Yan
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications UK Ltd 01.09.2019
• Subjects: Actin; Biotechnology; Cell culture; Cell Line; Cell Survival; Chronic illnesses; E-cadherin; Epithelial-Mesenchymal Transition; Epithelium - metabolism; Epithelium - pathology; Fibrosis; Humans; Immunofluorescence; Kidney diseases; Kidney Failure, Chronic - complications; Kidney Failure, Chronic - metabolism; Kidney Failure, Chronic - pathology; MAP kinase; Mesenchyme; Oxidative stress; Peritoneal dialysis; Peritoneal Fibrosis - etiology; Peritoneal Fibrosis - metabolism; Peritoneal Fibrosis - pathology; Peritoneum; Peritoneum - metabolism; Peritoneum - pathology; Polymerase chain reaction; Protein kinase; Reverse transcription; Signal Transduction; Smad3 Protein - metabolism; Smooth muscle; Studies; Transforming growth factor; Transforming Growth Factor beta1 - metabolism; Uric acid; Uric Acid - metabolism; Vimentin; United States > US; China
• ISSN: 1791-2997; 1791-3004
• DOI: 10.3892/mmr.2019.10476

Long‑term peritoneal dialysis is often limited or interrupted due to the development and progression of peritoneal fibrosis. Accumulating evidence suggests that epithelial‑mesenchymal transition (EMT) is a major component of peritoneal injury associated with peritoneal fibrosis in the end stage of renal disease; however, at present, the underlying mechanisms remain unclear. Thus, in the present study, uric acid (UA)‑induced EMT of peritoneal mesothelial cells was investigated by western‑blot and immunofluorescence staining. The results revealed that peritoneal mesothelial cells stimulated with UA underwent EMT, as demonstrated by the decreased expression of epithelial markers (E‑cadherin) and an increased expression of mesenchymal markers (α‑smooth muscle actin and vimentin). Additionally, it was reported that UA could facilitate the progression of EMT of peritoneal mesothelial cells via EMT transcription pathways, including transforming growth factor‑β1/mothers against decapentaplegic homolog 3 and P38/mitogen‑activated protein kinase by western‑blot and reverse transcription semi‑quantitative polymerase chain reaction. The results of the present study suggest that UA could promote EMT and may contribute to peritoneal chronic disease. Furthermore, the data obtained suggest that the levels of blood UA may account for the development of EMT; thus, lowering the levels of blood UA may be beneficial to inhibit the occurrence and development of peritoneal fibrosis.