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논문분류	춘계학술대회 초록집
제목	Effects of Transglutaminase 2 Inhibition on Peritoneal Fibrosis
저자	Jung Nam An
출판정보	2025; 2025(1):
키워드	Transglutaminase 2, Peritoneal fibrosis, TG2 inhibition
초록	Peritoneal fibrosis is a major cause of peritoneal dialysis failure. Transglutaminase 2 (TG2) regulates various biological processes and is related to arteriosclerosis and fibrosis. We aimed to clarify the role of TG2 in the mechanism of peritoneal fibrosis, demonstrate the protective effect of mesothelial cells through its inhibition, and search for effective molecules involved in TG2 activation. A peritoneal fibrosis animal model was established by intraperitoneal administration of 0.1% chlorhexidine gluconate solution at 3-day intervals for up to 30 days. In the cell model, human peritoneal mesothelial cells (HPMC) cultured primarily from the peritoneal fluid of peritoneal dialysis patients were treated with TGF-β (2 ng/ml) and TG2 inhibitor. The expression of TG2 was increased in the peritoneal tissue mRNA of the peritoneal fibrosis model, and the peritoneal tissue proteome analysis using ultra-high-resolution mass spectrometry also confirmed that the expression of TG2 protein was significantly increased. It was revealed that proteins mainly associated with cell-to-cell adhesion formed a close network with TG2. When TG2 inhibitor was treated for 48 hours in a peritoneal fibrosis cell model, the cell morphological and structural damage accompanied by TGF-β were recovered in a dose-dependent manner. The protein expression of fibronectin and IL-6 was also decreased. In addition, TG2 expression was confirmed in a peritoneal fibrosis model established by treating with glucose solution for 48 hours, and FN and NOX2 decreased together after TG2 inhibition. In particular, NOX2 was significantly reduced even at a low dose of inhibitor, suggesting the possibility that NOX2 is involved in the mechanism of TG2. We established animal and cell models of peritoneal fibrosis, elucidated its association with TG2, and identified a network between TG2 and cell-to-cell adhesion protein. Furthermore, we demonstrated improvement in cell shape and structure, and fibrosis and inflammation-related markers by TG2 inhibition.
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