Abstract：
:Peritoneal fibrosis (PF) is a severe complication of peritoneal dialysis, but there are few effective therapies for it. Recent studies have revealed a new biological function of trehalose as an autophagy inducer. Thus far, there are few reports regarding the therapeutic effects of trehalose on fibrotic diseases. Therefore, we examined whether trehalose has anti-fibrotic effects on PF. PF was induced by intraperitoneal injection of chlorhexidine gluconate (CG). CG challenges induced the increase of peritoneal thickness, ColIα1 mRNA expression and hydroxyproline content, all of which were significantly attenuated by trehalose. In addition, CG challenges induced a marked peritoneal accumulation of α-SMA+ myofibroblasts that was reduced by trehalose. The number of Wt1+ α-SMA+ cells in the peritoneum increased following CG challenges, suggesting that a part of α-SMA+ myofibroblasts were derived from peritoneal mesothelial cells (PMCs). The number of Wt1+ α-SMA+ cells was also suppressed by trehalose. Additionally, trehalose attenuated the increase of α-SMA and ColIα1 mRNA expression induced by TGF-β1 through Snail protein degradation, which was dependent on autophagy in PMCs. These results suggest that trehalose might be a novel therapeutic agent for PF through the induction of autophagy and the suppression of mesothelial-to-mesenchymal transition in PMCs.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Miyake T,Sakai N,Tamai A,Sato K,Kamikawa Y,Miyagawa T,Ogura H,Yamamura Y,Oshima M,Nakagawa S,Sagara A,Shinozaki Y,Toyama T,Kitajima S,Hara A,Iwata Y,Shimizu M,Furuichi K,Kaneko S,Wada Tdoi
10.1038/s41598-020-71230-4subject
Has Abstractpub_date
2020-08-31 00:00:00pages
14292issue
1issn
2045-2322pii
10.1038/s41598-020-71230-4journal_volume
10pub_type
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