ST2 blockade mitigates peritoneal fibrosis induced by TGF‐β and high glucose

Peritoneal fibrosis (PF) is an intractable complication of peritoneal dialysis (PD) that leads to peritoneal membrane failure. This study investigated the role of suppression of tumorigenicity (ST)2 in PF using patient samples along with mouse and cell‐based models. Baseline dialysate soluble (s)ST2...

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Published inJournal of cellular and molecular medicine Vol. 23; no. 10; pp. 6872 - 6884
Main Authors Kim, Yong Chul, Kim, Kyu Hong, Lee, Sunhwa, Jo, Ji‐won, Park, Jae Yoon, Park, Mi‐seon, Tsogbadrakh, Bodokhsuren, Lee, Jung Pyo, Lee, Jae Wook, Kim, Dong Ki, Oh, Kook‐Hwan, Jang, In‐Jin, Kim, Yon Su, Cha, Ran‐hui, Yang, Seung Hee
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.10.2019
John Wiley and Sons Inc
Subjects
Animal models
Animals
Biomarkers
Cell culture
Cells, Cultured
Chlorhexidine
Disease Models, Animal
Effluents
Epithelial-Mesenchymal Transition - drug effects
Epithelium - pathology
Female
Fibroblasts
Fibronectin
Fibrosis
Gene expression
Glucose - toxicity
Growth factors
Heart attacks
Hemodialysis
Humans
Inflammation
Interleukin-1 Receptor-Like 1 Protein - antagonists & inhibitors
Interleukin-1 Receptor-Like 1 Protein - metabolism
Male
Mice, Inbred C57BL
Mice, Knockout
Middle Aged
Original
Peritoneal Dialysis
peritoneal fibrosis
Peritoneal Fibrosis - pathology
Peritoneum
Peritoneum - pathology
Preservation
Proportional Hazards Models
Snail protein
soluble ST2
ST2 blockade
Survival Analysis
Transforming Growth Factor beta - toxicity
Transforming growth factor-b
Tumorigenicity
β-Galactosidase
peritoneal fibrosis
ST2 blockade
peritoneal dialysis
soluble ST2
Online AccessGet full text

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Abstract Peritoneal fibrosis (PF) is an intractable complication of peritoneal dialysis (PD) that leads to peritoneal membrane failure. This study investigated the role of suppression of tumorigenicity (ST)2 in PF using patient samples along with mouse and cell‐based models. Baseline dialysate soluble (s)ST2 level in patients measured 1 month after PD initiation was 2063.4 ± 2457.8 pg/mL; patients who switched to haemodialysis had elevated sST2 levels in peritoneal effluent (1576.2 ± 199.9 pg/mL, P = .03), which was associated with PD failure (P = .04). Baseline sST2 showed good performance in predicting PD failure (area under the receiver operating characteristic curve = 0.780, P = .001). In mice with chlorhexidine gluconate‐induced PF, ST2 was expressed in fibroblasts and mesothelial cells within submesothelial zones. In primary cultured human peritoneal mesothelial cells (HPMCs), transforming growth factor‐β treatment increased ST2, fibronectin, β‐galactosidase and Snail protein levels and decreased E‐cadherin level. Anti‐ST2 antibody administration reversed the up‐regulation of ST2 and fibronectin expression; it also reduced fibrosis induced by high glucose (100 mmol/L) in HPMCs. Thus, high ST2 level in dialysate is a marker for fibrosis and inflammation during peritoneal injury, and blocking ST2 may be an effective therapeutic strategy for renal preservation.
AbstractList Peritoneal fibrosis (PF) is an intractable complication of peritoneal dialysis (PD) that leads to peritoneal membrane failure. This study investigated the role of suppression of tumorigenicity (ST)2 in PF using patient samples along with mouse and cell‐based models. Baseline dialysate soluble (s)ST2 level in patients measured 1 month after PD initiation was 2063.4 ± 2457.8 pg/mL; patients who switched to haemodialysis had elevated sST2 levels in peritoneal effluent (1576.2 ± 199.9 pg/mL, P  = .03), which was associated with PD failure ( P  = .04). Baseline sST2 showed good performance in predicting PD failure (area under the receiver operating characteristic curve = 0.780, P  = .001). In mice with chlorhexidine gluconate‐induced PF, ST2 was expressed in fibroblasts and mesothelial cells within submesothelial zones. In primary cultured human peritoneal mesothelial cells (HPMCs), transforming growth factor‐β treatment increased ST2, fibronectin, β‐galactosidase and Snail protein levels and decreased E‐cadherin level. Anti‐ST2 antibody administration reversed the up‐regulation of ST2 and fibronectin expression; it also reduced fibrosis induced by high glucose (100 mmol/L) in HPMCs. Thus, high ST2 level in dialysate is a marker for fibrosis and inflammation during peritoneal injury, and blocking ST2 may be an effective therapeutic strategy for renal preservation.
Peritoneal fibrosis (PF) is an intractable complication of peritoneal dialysis (PD) that leads to peritoneal membrane failure. This study investigated the role of suppression of tumorigenicity (ST)2 in PF using patient samples along with mouse and cell-based models. Baseline dialysate soluble (s)ST2 level in patients measured 1 month after PD initiation was 2063.4 ± 2457.8 pg/mL; patients who switched to haemodialysis had elevated sST2 levels in peritoneal effluent (1576.2 ± 199.9 pg/mL, P = .03), which was associated with PD failure (P = .04). Baseline sST2 showed good performance in predicting PD failure (area under the receiver operating characteristic curve = 0.780, P = .001). In mice with chlorhexidine gluconate-induced PF, ST2 was expressed in fibroblasts and mesothelial cells within submesothelial zones. In primary cultured human peritoneal mesothelial cells (HPMCs), transforming growth factor-β treatment increased ST2, fibronectin, β-galactosidase and Snail protein levels and decreased E-cadherin level. Anti-ST2 antibody administration reversed the up-regulation of ST2 and fibronectin expression; it also reduced fibrosis induced by high glucose (100 mmol/L) in HPMCs. Thus, high ST2 level in dialysate is a marker for fibrosis and inflammation during peritoneal injury, and blocking ST2 may be an effective therapeutic strategy for renal preservation.Peritoneal fibrosis (PF) is an intractable complication of peritoneal dialysis (PD) that leads to peritoneal membrane failure. This study investigated the role of suppression of tumorigenicity (ST)2 in PF using patient samples along with mouse and cell-based models. Baseline dialysate soluble (s)ST2 level in patients measured 1 month after PD initiation was 2063.4 ± 2457.8 pg/mL; patients who switched to haemodialysis had elevated sST2 levels in peritoneal effluent (1576.2 ± 199.9 pg/mL, P = .03), which was associated with PD failure (P = .04). Baseline sST2 showed good performance in predicting PD failure (area under the receiver operating characteristic curve = 0.780, P = .001). In mice with chlorhexidine gluconate-induced PF, ST2 was expressed in fibroblasts and mesothelial cells within submesothelial zones. In primary cultured human peritoneal mesothelial cells (HPMCs), transforming growth factor-β treatment increased ST2, fibronectin, β-galactosidase and Snail protein levels and decreased E-cadherin level. Anti-ST2 antibody administration reversed the up-regulation of ST2 and fibronectin expression; it also reduced fibrosis induced by high glucose (100 mmol/L) in HPMCs. Thus, high ST2 level in dialysate is a marker for fibrosis and inflammation during peritoneal injury, and blocking ST2 may be an effective therapeutic strategy for renal preservation.
Peritoneal fibrosis (PF) is an intractable complication of peritoneal dialysis (PD) that leads to peritoneal membrane failure. This study investigated the role of suppression of tumorigenicity (ST)2 in PF using patient samples along with mouse and cell‐based models. Baseline dialysate soluble (s)ST2 level in patients measured 1 month after PD initiation was 2063.4 ± 2457.8 pg/mL; patients who switched to haemodialysis had elevated sST2 levels in peritoneal effluent (1576.2 ± 199.9 pg/mL, P = .03), which was associated with PD failure (P = .04). Baseline sST2 showed good performance in predicting PD failure (area under the receiver operating characteristic curve = 0.780, P = .001). In mice with chlorhexidine gluconate‐induced PF, ST2 was expressed in fibroblasts and mesothelial cells within submesothelial zones. In primary cultured human peritoneal mesothelial cells (HPMCs), transforming growth factor‐β treatment increased ST2, fibronectin, β‐galactosidase and Snail protein levels and decreased E‐cadherin level. Anti‐ST2 antibody administration reversed the up‐regulation of ST2 and fibronectin expression; it also reduced fibrosis induced by high glucose (100 mmol/L) in HPMCs. Thus, high ST2 level in dialysate is a marker for fibrosis and inflammation during peritoneal injury, and blocking ST2 may be an effective therapeutic strategy for renal preservation.
Peritoneal fibrosis (PF) is an intractable complication of peritoneal dialysis (PD) that leads to peritoneal membrane failure. This study investigated the role of suppression of tumorigenicity (ST)2 in PF using patient samples along with mouse and cell-based models. Baseline dialysate soluble (s)ST2 level in patients measured 1 month after PD initiation was 2063.4 ± 2457.8 pg/mL; patients who switched to haemodialysis had elevated sST2 levels in peritoneal effluent (1576.2 ± 199.9 pg/mL, P = .03), which was associated with PD failure (P = .04). Baseline sST2 showed good performance in predicting PD failure (area under the receiver operating characteristic curve = 0.780, P = .001). In mice with chlorhexidine gluconate-induced PF, ST2 was expressed in fibroblasts and mesothelial cells within submesothelial zones. In primary cultured human peritoneal mesothelial cells (HPMCs), transforming growth factor-β treatment increased ST2, fibronectin, β-galactosidase and Snail protein levels and decreased E-cadherin level. Anti-ST2 antibody administration reversed the up-regulation of ST2 and fibronectin expression; it also reduced fibrosis induced by high glucose (100 mmol/L) in HPMCs. Thus, high ST2 level in dialysate is a marker for fibrosis and inflammation during peritoneal injury, and blocking ST2 may be an effective therapeutic strategy for renal preservation.
Author Jang, In‐Jin
Kim, Yon Su
Kim, Dong Ki
Lee, Sunhwa
Park, Jae Yoon
Yang, Seung Hee
Lee, Jung Pyo
Park, Mi‐seon
Cha, Ran‐hui
Kim, Yong Chul
Tsogbadrakh, Bodokhsuren
Jo, Ji‐won
Lee, Jae Wook
Oh, Kook‐Hwan
Kim, Kyu Hong
AuthorAffiliation 10 Department of Medical Science Seoul National University College of Medicine Seoul Korea
6 Department of Internal Medicine Seoul National University College of Medicine Seoul Korea
2 Department of Microbiology The Ohio State University Columbus OH USA
3 Biomedical Research Institute, Seoul National University Hospital Seoul Korea
7 Nephrology Clinic National Cancer Center Ilsan Korea
8 Kidney Research Institute, Seoul National University Seoul Korea
1 Department of Internal Medicine Seoul National University Hospital Seoul Korea
9 Department of Clinical Pharmacology and Therapeutics Seoul National University College of Medicine and Hospital Seoul Korea
11 Division of Nephrology, Department of Internal Medicine National Medical Center Seoul Korea
4 Department of Internal Medicine Dongguk University Ilsan Hospital Gyeonggi‐do Korea
5 Department of Internal Medicine Seoul National University Boramae Medical Center Seoul Korea
AuthorAffiliation_xml – name: 9 Department of Clinical Pharmacology and Therapeutics Seoul National University College of Medicine and Hospital Seoul Korea
– name: 2 Department of Microbiology The Ohio State University Columbus OH USA
– name: 11 Division of Nephrology, Department of Internal Medicine National Medical Center Seoul Korea
– name: 1 Department of Internal Medicine Seoul National University Hospital Seoul Korea
– name: 4 Department of Internal Medicine Dongguk University Ilsan Hospital Gyeonggi‐do Korea
– name: 8 Kidney Research Institute, Seoul National University Seoul Korea
– name: 10 Department of Medical Science Seoul National University College of Medicine Seoul Korea
– name: 5 Department of Internal Medicine Seoul National University Boramae Medical Center Seoul Korea
– name: 3 Biomedical Research Institute, Seoul National University Hospital Seoul Korea
– name: 6 Department of Internal Medicine Seoul National University College of Medicine Seoul Korea
– name: 7 Nephrology Clinic National Cancer Center Ilsan Korea
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Copyright 2019 The Authors. published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
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Issue 10
Keywords peritoneal fibrosis
ST2 blockade
peritoneal dialysis
soluble ST2
Language English
License Attribution
2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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Notes Funding information
This research was supported by grants from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute funded by the Ministry of Health & Welfare, Republic of Korea (no. NRF‐2017R1A2B2009518), and the National Medical Center, Seoul, Republic of Korea (no. NMC2017‐MS‐06).
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PublicationDate_xml – month: 10
  year: 2019
  text: October 2019
PublicationDecade 2010
PublicationPlace England
PublicationPlace_xml – name: England
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PublicationTitle Journal of cellular and molecular medicine
PublicationTitleAlternate J Cell Mol Med
PublicationYear 2019
Publisher John Wiley & Sons, Inc
John Wiley and Sons Inc
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– name: John Wiley and Sons Inc
References 2007; 18
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Snippet Peritoneal fibrosis (PF) is an intractable complication of peritoneal dialysis (PD) that leads to peritoneal membrane failure. This study investigated the role...
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pubmed
crossref
wiley
SourceType Open Access Repository
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StartPage 6872
SubjectTerms Animal models
Animals
Biomarkers
Cell culture
Cells, Cultured
Chlorhexidine
Disease Models, Animal
Effluents
Epithelial-Mesenchymal Transition - drug effects
Epithelium - pathology
Female
Fibroblasts
Fibronectin
Fibrosis
Gene expression
Glucose - toxicity
Growth factors
Heart attacks
Hemodialysis
Humans
Inflammation
Interleukin-1 Receptor-Like 1 Protein - antagonists & inhibitors
Interleukin-1 Receptor-Like 1 Protein - metabolism
Male
Mice, Inbred C57BL
Mice, Knockout
Middle Aged
Original
Peritoneal Dialysis
peritoneal fibrosis
Peritoneal Fibrosis - pathology
Peritoneum
Peritoneum - pathology
Preservation
Proportional Hazards Models
Snail protein
soluble ST2
ST2 blockade
Survival Analysis
Transforming Growth Factor beta - toxicity
Transforming growth factor-b
Tumorigenicity
β-Galactosidase
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Title ST2 blockade mitigates peritoneal fibrosis induced by TGF‐β and high glucose
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcmm.14571
https://www.ncbi.nlm.nih.gov/pubmed/31397957
https://www.proquest.com/docview/2303551763
https://www.proquest.com/docview/2271853859
https://pubmed.ncbi.nlm.nih.gov/PMC6787438
Volume 23
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