Inhibition of Transglutaminase 2 Reduces Peritoneal Injury in a Chlorhexidine-Induced Peritoneal Fibrosis Model
Long-term peritoneal dialysis (PD) is often associated with peritoneal dysfunction leading to withdrawal from PD. The characteristic pathologic features of peritoneal dysfunction are widely attributed to peritoneal fibrosis and angiogenesis. The detailed mechanisms remain unclear, and treatment targ...
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Published in | Laboratory investigation Vol. 103; no. 4; p. 100050 |
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Main Authors | , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier Inc
01.04.2023
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Abstract | Long-term peritoneal dialysis (PD) is often associated with peritoneal dysfunction leading to withdrawal from PD. The characteristic pathologic features of peritoneal dysfunction are widely attributed to peritoneal fibrosis and angiogenesis. The detailed mechanisms remain unclear, and treatment targets in clinical settings have yet to be identified. We investigated transglutaminase 2 (TG2) as a possible novel therapeutic target for peritoneal injury. TG2 and fibrosis, inflammation, and angiogenesis were investigated in a chlorhexidine gluconate (CG)-induced model of peritoneal inflammation and fibrosis, representing a noninfectious model of PD-related peritonitis. Transforming growth factor (TGF)-β type I receptor (TGFβR-I) inhibitor and TG2-knockout mice were used for TGF-β and TG2 inhibition studies, respectively. Double immunostaining was performed to identify cells expressing TG2 and endothelial-mesenchymal transition (EndMT). In the rat CG model of peritoneal fibrosis, in situ TG2 activity and protein expression increased during the development of peritoneal fibrosis, as well as increases in peritoneal thickness and numbers of blood vessels and macrophages. TGFβR-I inhibitor suppressed TG2 activity and protein expression, as well as peritoneal fibrosis and angiogenesis. TGF-β1 expression, peritoneal fibrosis, and angiogenesis were suppressed in TG2-knockout mice. TG2 activity was detected by α-smooth muscle actin-positive myofibroblasts, CD31-positive endothelial cells, and ED-1-positive macrophages. CD31-positive endothelial cells in the CG model were α-smooth muscle actin-positive, vimentin-positive, and vascular endothelial-cadherin-negative, suggesting EndMT. In the CG model, EndMT was suppressed in TG2-knockout mice. TG2 was involved in the interactive regulation of TGF-β. As inhibition of TG2 reduced peritoneal fibrosis, angiogenesis, and inflammation associated with TGF-β and vascular endothelial growth factor-A suppression, TG2 may provide a new therapeutic target for ameliorating peritoneal injuries in PD. |
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AbstractList | Long-term peritoneal dialysis (PD) is often associated with peritoneal dysfunction leading to withdrawal from PD. The characteristic pathologic features of peritoneal dysfunction are widely attributed to peritoneal fibrosis and angiogenesis. The detailed mechanisms remain unclear, and treatment targets in clinical settings have yet to be identified. We investigated transglutaminase 2 (TG2) as a possible novel therapeutic target for peritoneal injury. TG2 and fibrosis, inflammation, and angiogenesis were investigated in a chlorhexidine gluconate (CG)-induced model of peritoneal inflammation and fibrosis, representing a noninfectious model of PD-related peritonitis. Transforming growth factor (TGF)-β type I receptor (TGFβR-I) inhibitor and TG2-knockout mice were used for TGF-β and TG2 inhibition studies, respectively. Double immunostaining was performed to identify cells expressing TG2 and endothelial-mesenchymal transition (EndMT). In the rat CG model of peritoneal fibrosis, in situ TG2 activity and protein expression increased during the development of peritoneal fibrosis, as well as increases in peritoneal thickness and numbers of blood vessels and macrophages. TGFβR-I inhibitor suppressed TG2 activity and protein expression, as well as peritoneal fibrosis and angiogenesis. TGF-β1 expression, peritoneal fibrosis, and angiogenesis were suppressed in TG2-knockout mice. TG2 activity was detected by α-smooth muscle actin-positive myofibroblasts, CD31-positive endothelial cells, and ED-1-positive macrophages. CD31-positive endothelial cells in the CG model were α-smooth muscle actin-positive, vimentin-positive, and vascular endothelial-cadherin-negative, suggesting EndMT. In the CG model, EndMT was suppressed in TG2-knockout mice. TG2 was involved in the interactive regulation of TGF-β. As inhibition of TG2 reduced peritoneal fibrosis, angiogenesis, and inflammation associated with TGF-β and vascular endothelial growth factor-A suppression, TG2 may provide a new therapeutic target for ameliorating peritoneal injuries in PD. |
ArticleNumber | 100050 |
Author | Mizuno, Masashi Tatsukawa, Hideki Hitomi, Kiyotaka Sakai, Yukinao Kinashi, Hiroshi Ishimoto, Takuji Takeuchi, Kosei Ito, Yasuhiko Kunoki, Shunnosuke Suzuki, Yasuhiro Yamaguchi, Makoto Sasakura, Hiroyuki Kariya, Tetsuyoshi Ikeno, Masashi |
Author_xml | – sequence: 1 givenname: Shunnosuke surname: Kunoki fullname: Kunoki, Shunnosuke organization: Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan – sequence: 2 givenname: Hideki surname: Tatsukawa fullname: Tatsukawa, Hideki organization: Cellular Biochemistry Lab, Graduate School of Pharmaceutical Sciences, Nagoya University, Nagoya, Japan – sequence: 3 givenname: Yukinao surname: Sakai fullname: Sakai, Yukinao organization: Department of Nephrology, Nippon Medical School, Tokyo, Japan – sequence: 4 givenname: Hiroshi surname: Kinashi fullname: Kinashi, Hiroshi organization: Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan – sequence: 5 givenname: Tetsuyoshi surname: Kariya fullname: Kariya, Tetsuyoshi organization: Department of Nephrology, Nagoya University, Nagoya, Japan – sequence: 6 givenname: Yasuhiro surname: Suzuki fullname: Suzuki, Yasuhiro organization: Department of Nephrology, Nagoya University, Nagoya, Japan – sequence: 7 givenname: Masashi surname: Mizuno fullname: Mizuno, Masashi organization: Department of Nephrology, Nagoya University, Nagoya, Japan – sequence: 8 givenname: Makoto surname: Yamaguchi fullname: Yamaguchi, Makoto organization: Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan – sequence: 9 givenname: Hiroyuki surname: Sasakura fullname: Sasakura, Hiroyuki organization: Department of Medical Cell Biology, Aichi Medical University, Nagakute, Aichi, Japan – sequence: 10 givenname: Masashi surname: Ikeno fullname: Ikeno, Masashi organization: Department of Medical Cell Biology, Aichi Medical University, Nagakute, Aichi, Japan – sequence: 11 givenname: Kosei surname: Takeuchi fullname: Takeuchi, Kosei organization: Department of Medical Cell Biology, Aichi Medical University, Nagakute, Aichi, Japan – sequence: 12 givenname: Takuji surname: Ishimoto fullname: Ishimoto, Takuji organization: Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan – sequence: 13 givenname: Kiyotaka surname: Hitomi fullname: Hitomi, Kiyotaka organization: Cellular Biochemistry Lab, Graduate School of Pharmaceutical Sciences, Nagoya University, Nagoya, Japan – sequence: 14 givenname: Yasuhiko orcidid: 0000-0002-9676-6961 surname: Ito fullname: Ito, Yasuhiko email: yasuito@aichi-med-u.ac.jp organization: Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan |
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Keywords | peritoneal fibrosis α-SMA transglutaminase TGF-β1 EndMT chlorhexidine-induced model |
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SubjectTerms | Actins - metabolism Animals Chlorhexidine - adverse effects Chlorhexidine - metabolism chlorhexidine-induced model EndMT Endothelial Cells - metabolism Fibrosis Inflammation - metabolism Mice Mice, Knockout peritoneal fibrosis Peritoneal Fibrosis - chemically induced Peritoneal Fibrosis - metabolism Peritoneal Fibrosis - prevention & control Peritoneum - pathology Protein Glutamine gamma Glutamyltransferase 2 Rats TGF-β1 Transforming Growth Factor beta - metabolism Transforming Growth Factor beta1 - metabolism transglutaminase Vascular Endothelial Growth Factor A - metabolism α-SMA |
Title | Inhibition of Transglutaminase 2 Reduces Peritoneal Injury in a Chlorhexidine-Induced Peritoneal Fibrosis Model |
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