Inhibitory Effect of Mongolian Medicine Yihe Decoction on Inflammatory Reaction and Fibrosis of Human Peritoneal Mesothelial Cells Induced by High Glucose in Vitro

2019 ◽  
Vol 08 (03) ◽  
pp. 233-237
Author(s):  
根 巴
2011 ◽  
Vol 34 (6) ◽  
pp. 489-494 ◽  
Author(s):  
Marta Ciszewicz ◽  
George Wu ◽  
Paul Tam ◽  
Alicja Połubinska ◽  
Andrzej Bręborowicz

2015 ◽  
Vol 20 (1) ◽  
pp. 30-38 ◽  
Author(s):  
Keiko Kokoroishi ◽  
Ayumu Nakashima ◽  
Shigehiro Doi ◽  
Toshinori Ueno ◽  
Toshiki Doi ◽  
...  

2004 ◽  
Vol 24 (2) ◽  
pp. 147-155 ◽  
Author(s):  
Susan Yung ◽  
Heinz Hausser ◽  
Gareth Thomas ◽  
Liliana Schaefer ◽  
Hans Kresse ◽  
...  

Objective Previous studies have shown that decorin and biglycan account for over 70% of the proteoglycans (PGs) synthesized by human peritoneal mesothelial cells (HPMCs). Since these PGs are involved in the control of cell growth, cell differentiation, and matrix assembly, we investigated their turnover in cultured HPMCs. Methods Confluent HPMCs were metabolically labeled with [35S]-sulfate and the labeled products isolated from the cell medium and the cell layer characterized by sensitivity to bacterial eliminases. Experiments were undertaken with exogenous labeled decorin, and its metabolic state was studied. Results In a 24-hour labeling period, 75% of the newly synthesized chondroitin sulfate/dermatan sulfate (CS/DS) PGs appeared in the culture medium, the majority of which (90%) was decorin. In the cell layer, protein-free glycosaminoglycan (GAG) chains accounted for 21% of the total CS/DS at 24 hours and exhibited constant specific activity at 12 – 16 hours. The latter material was turned over with a half-life of approximately 2.5 hours. Exogenous decorin underwent receptor-mediated endocytosis and subsequent intracellular degradation. Uptake but not degradation could be inhibited by heparin. Conclusions HPMCs are distinguished by a rapid turnover of decorin. A characteristic metabolic feature is the existence of a large intracellular pool of protein-free DS-GAGs. Understanding the control of decorin turnover in HPMCs might lead to delineation of its potential role in both the physiology and pathophysiology of the membrane in PD patients.


2002 ◽  
Vol 62 (4) ◽  
pp. 1431-1439 ◽  
Author(s):  
Kar Neng Lai ◽  
Joseph C.K. Leung ◽  
Loretta Y.Y. Chan ◽  
Sydney Tang ◽  
Fu Keung Li ◽  
...  

1994 ◽  
Vol 3 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Apollo Pronk ◽  
Arthur A.G.M. Hoynck Van Papendrecht ◽  
Piet Leguit ◽  
Henri A. Verbrugh ◽  
Roel P.A.J. Verkooyen ◽  
...  

Cell seeding may decrease the thrombogenicity of implanted vascular grafts, but its application is hampered by the limited availability of autologous endothelial cells. Human peritoneal mesothelial cells have blood flow supporting qualities and are readily available. This study investigated the adherence of mesothelial cells to vascular prostheses and their subsequent growth in vitro. Circular pieces of various vascular prosthetic materials were seeded with 51Chromium-labeled mesothelial and endothelial cells and left for either 5, 15, 30, 60, and 120 minutes. The unattached cells were removed and the degree of cell attachment was measured. The number of mesothelial cells to Dacron increased during the first 60 min up to 35.2 % of the seeded inoculum whereafter a plateau was reached. Scanning electron microscopy showed spreaded mesothelial cells adherent to the Dacron fibers. A significant increase in adherence was observed after preincubation of Dacron with 10 μg/mL fibronectin, but no improvement was found after preincubation with human serum albumin or gelatin. Mesothelial cells adhered better to Gelcoated than to Gelsealed or plain Dacron. The adherence of mesothelial cells to ePTFE (Teflon) was significantly poorer. No significant differences in adherence were found between mesothelial and endothelial cells. Mesothelial cell growth on Dacron resulted in a modest increase in the number of viable cells during 27 days, which implies biocompatibility of Dacron and mesothelial cells in vitro.


2005 ◽  
Vol 28 (2) ◽  
pp. 141-149 ◽  
Author(s):  
Y. Naiki ◽  
K. Matsuo ◽  
T. Matsuoka ◽  
Y. Maeda

Human peritoneal mesothelial cells (HPMCs) play an important role in peritoneal functions. During long term peritoneal dialysis, it has been reported that HPMCs are damaged by high glucose solution via the signal of transforming growth factor (TGF)- ß1 produced by HPMCs. In this study, we focused on the effect of hepatocyte growth factor (HGF), known as an anti-fibrotic and anti-TGF-ß1 agent, on HPMCs damaged by high glucose solution. HPMCs were isolated from specimens of the omentum from nonuremic patients after informed consent had been obtained. After confirming adhesion for 6 hours, 100 μL of DMEM with 0.5%FCS were added at different concentrations (D-glucose; 6, 30mM) with or without HGF (10, 30, 100 ng/mL) for 48 hours. We examined the effects of a high concentration of glucose and then focused on following four critical points: 1) the production of HGF from HPMCs exposed to a high concentration of glucose, 2) the expression of c-Met on HPMCs, 3) the viability of those cells, and 4) matrix metalloproteinase-2 (MMP-2) and tissue inhibitors of metalloproteinase-2 (TIMP-2). The following significant changes are described herein: high glucose solution and TGF-ß1 i) decreased HGF production from HPMCs and ii) up-regulated expression of c-Met on HPMCs, and addition of HGF iii) restored viability of HPMCs damaged by glucose, iv) suppressed TGF-ß1 production by HGF, and v) induced up-regulation of MMP-2 and decreased TIMP-2 production by HPMCs. Levels of HGF decreased by high concentrations of glucose in the peritoneal cavity may induce the loss of HPMCs and thereby result in peritoneal fibrosis. These results suggest that HGF is an effective agent in the regeneration of peritoneal membrane damaged by high glucose solution.


2006 ◽  
Vol 26 (3) ◽  
pp. 393-401 ◽  
Author(s):  
Miyuki Shimizu ◽  
Yoshitaka Ishibashi ◽  
Fumika Taki ◽  
Hideki Shimizu ◽  
Ichiro Hirahara ◽  
...  

Background Long-term peritoneal dialysis using glucose-based dialysates is associated with peritoneal fibrosis. The object of this study was to investigate the hypothesis that endothelin (ET)-1, which is known to play an important role in various fibrotic diseases, may also be involved in peritoneal fibrosis using human peritoneal mesothelial cells (HPMC). Methods HPMC were cultured with 4% d- or l-glucose, or loaded with 10 nmol/L ET-1. In some experiments, the ETA receptor antagonist BQ-123, the ETB receptor antagonist BQ-788, and antioxidants 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (TEMPOL) and diphenyleneiodium chloride (DPI) were used. mRNA expression of ET-1, ETA receptor, ETB receptor, and fibronectin (FN) was analyzed by real-time polymerase chain reaction (real-time PCR). The protein levels for FN and ET-1 were measured by ELISA. CM-H2DCFDA-sensitive reactive oxygen species (ROS) were evaluated by flow cytometry. Results d-Glucose significantly induced mRNA expression of ET-1 and the ETB receptor but not the ETA receptor. FN production under high glucose conditions was inhibited by BQ-788. ET-1 directly stimulated HPMC to increase mRNA expression of FN and CM-H2DCFDA-sensitive ROS production. BQ-788, TEMPOL, and DPI inhibited mRNA expression of FN induced by ET-1. Conclusion The present study suggests that high-glucose-induced FN synthesis is mediated by the ET-1/ETB receptor pathway and, therefore, an ETB receptor antagonist may be useful in preventing FN production in HPMC.


2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Yuki Kimura ◽  
Hideyuki Ohzawa ◽  
Hideyo Miyato ◽  
Yuki Kaneko ◽  
Akira Saito ◽  
...  

AbstractPeritoneal dissemination is a major metastatic pathway for gastrointestinal and ovarian malignancies. The miR-29b family is downregulated in peritoneal fluids in patients with peritoneal metastases (PM). We examined the effect of miR-29b on mesothelial cells (MC) which play critical a role in the development of PM through mesothelial-mesenchymal transition (MMT). Human peritoneal mesothelial cells (HPMCs) were isolated from surgically resected omental tissue and MMT induced by stimulation with 10 ng/ml TGF-β1. MiR-29b mimics and negative control miR were transfected by lipofection using RNAiMAX and the effects on the MMT evaluated in vitro. HPMC produced substantial amounts of miR-29b which was markedly inhibited by TGF-β1. TGF-β1 stimulation of HPMC induced morphological changes with decreased expression of E-cadherin and calretinin, and increased expression of vimentin and fibronectin. TGF-β1 also enhanced proliferation and migration of HPMC as well as adhesion of tumor cells in a fibronectin dependent manner. However, all events were strongly abrogated by simultaneous transfection of miR-29b. MiR-29b inhibits TGF-β1 induced MMT and replacement of miR-29b in the peritoneal cavity might be effective to prevent development of PM partly through the effects on MC.


2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Ke Zhang ◽  
Hao Zhang ◽  
Xun Zhou ◽  
Wen-bin Tang ◽  
Li Xiao ◽  
...  

Background. microRNA (miRNA, miR) are thought to interact with multiple mRNAs which are involved in the EMT process. But the role of miRNAs in peritoneal fibrosis has remained unknown.Objective. To determine if miRNA589 regulates the EMT induced by TGFβ1 in human peritoneal mesothelial cell line (HMrSV5 cells).Methods. 1. Level of miR589 was detected in both human peritoneal mesothelial cells (HPMCs) isolated from continuous ambulatory peritoneal dialysis (CAPD) patients’ effluent and HMrSV5 cells treated with or without TGFβ1. 2. HMrSV5 cells were divided into three groups: control group, TGFβ1 group, and pre-miR-589+TGFβ1 group. The level of miRNA589 was determined by realtime PCR. The expressions of ZO-1, vimentin, and E-cadherin in HPMCs were detected, respectively.Results. Decreased level of miRNA589 was obtained in either HPMCs of long-term CAPD patients or HMrSV5 cells treated with TGFβ1. In vitro, TGFβ1 led to upregulation of vimentin and downregulation of ZO-1 as well as E-cadherin in HMrSV5 cells, which suggested EMT, was induced. The changes were accompanied with notably decreased level of miRNA589 in HMrSV5 cells treated with TGFβ1. Overexpression of miRNA589 by transfection with pre-miRNA589 partially reversed these EMT changes.Conclusion. miRNA589 mediates TGFβ1 induced EMT in human peritoneal mesothelial cells.


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