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Overexpression of glyoxalase 1 attenuates methylglyoxal‐induced peritoneal injury with suppression of epithelial mesenchymal transition pathway and neovascularization in Wistar rats
Author(s) -
Oba Ikuko,
Mori Takefumi,
Ohsaki Yusuke,
Sato Emiko,
Nakamichi Yoshimi,
Miyata Toshio,
Ito Sadayoshi
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.910.13
Subject(s) - methylglyoxal , peritoneum , intraperitoneal injection , medicine , neovascularization , immunohistochemistry , saline , lactoylglutathione lyase , mmp2 , fibrosis , endocrinology , pathology , chemistry , angiogenesis , biochemistry , cancer , metastasis , enzyme
Methylglyoxal (MG) is one of the causes of peritoneal injury in peritoneal dialysis. We have previously demonstrated that intraperitoneal administration of MG induced peritoneal fibrosis in Wistar rats, which was reduced in glyoxalase 1 transgenic (GLO1‐Tg) rats. Present study was designed to evaluate the contribution of Epithelial Mesenchymal Transition (EMT) in MG induced peritoneal injury. Twenty ml of 1 mM MG solution was intraperitoneally administered daily to either GLO1‐Tg rats or control Wistar rats for two weeks. Saline was administered as sham group. At the end of the study, liver was removed for immunohistochemical analysis of the peritoneum. α‐SMA, TGF‐β and MMP2 expressions in the peritoneum fibrotic region of Wistar rats compared to those of sham group, which was reduced in GLO1‐Tg rats. Neovascularization determined by Von Willebrand factor staining with increased VEGF expression was observed in the peritoneal fibrotic lesion of MG treated Wistar rats compared to sham group, which was reduced in those of GLO1‐Tg rats. Peritoneal GLO1 expression was increased in GLO1‐Tg rats compared to those of Wistar rats. We conclude that MG induces peritoneal injury with enhanced EMT and neovascularization, which was attenuated by overexpression of GLO1.