Intraperitoneal Cefazolin and Ceftazidime Effects on Human Peritoneal Mesothelial Cell Release of Cancer Antigen–125

2004 ◽  
Vol 38 (12) ◽  
pp. 2035-2040
Author(s):  
Harold J Manley ◽  
Rowland J Elwell ◽  
George R Bailie ◽  
Charles L Welch
Keyword(s):  
Mesothelial Cell ◽  
Cancer Antigen 125 ◽  
Cancer Antigen ◽  
Cell Release ◽  
Peritoneal Mesothelial Cell ◽  
Human Peritoneal Mesothelial Cell

scholarly journals Pentoxifylline inhibits human peritoneal mesothelial cell growth and collagen synthesis: Effects on TGF-β

2000 ◽  
Vol 57 (6) ◽  
pp. 2626-2633 ◽  
Author(s):  
Cheng-Chung Fang ◽  
Chung-Jen Yen ◽  
Yung-Ming Chen ◽  
Ren-Shi Shyu ◽  
Tun-Jun Tsai ◽  
...  
Keyword(s):  
Cell Growth ◽  
Collagen Synthesis ◽  
Mesothelial Cell ◽  
Peritoneal Mesothelial Cell ◽  
Human Peritoneal Mesothelial Cell

scholarly journals Effect of Glucose Degradation Products on Human Peritoneal Mesothelial Cell Function

2000 ◽  
Vol 11 (4) ◽  
pp. 729-739 ◽  
Author(s):  
JANUSZ WITOWSKI ◽  
KATARZYNA KORYBALSKA ◽  
JUSTYNA WISNIEWSKA ◽  
ANDRZEJ BREBOROWICZ ◽  
GERHARD M. GAHL ◽  
...  
Keyword(s):  
Cell Function ◽  
Degradation Products ◽  
Mesothelial Cell ◽  
L929 Cells ◽  
Glucose Degradation Products ◽  
Transformed Cell Lines ◽  
The Impact ◽  
Peritoneal Mesothelial Cell ◽  
Dialysis Fluids ◽  
Human Peritoneal Mesothelial Cell

Abstract. Bioincompatibility of conventional glucose-based peritoneal dialysis fluids (PDF) has been partially attributed to the presence of glucose degradation products (GDP) generated during heat sterilization of PDF. Most previous studies on GDP toxicity were performed on animal and/or transformed cell lines, and the impact of GDP on peritoneal cells remains obscure. The short-term effects of six identified GDP on human peritoneal mesothelial cell (HPMC) functions were examined in comparison to murine L929 fibroblasts. Exposure of HPMC to acetaldehyde, formaldehyde, glyoxal, methylglyoxal, furaldehyde, but not to 5-hydroxymethyl-furfural, resulted in dose-dependent inhibition of cell growth, viability, and interleukin-1 β (IL-1 β)-stimulated IL-6 release; for several GDP, this suppression was significantly greater compared with L929 cells. Although the addition of GDP to culture medium at concentrations found in PDF had no major impact on HPMC function, the exposure of HPMC to filter-sterilized PDF led to a significantly smaller suppression of HPMC proliferation compared to that induced by heat-sterilized PDF. The growth inhibition mediated by filter-sterilized PDF could be increased after the addition of clinically relevant doses of GDP. These effects were equally evident in L929 cells. In conclusion, GDP reveal a significant cytotoxic potential toward HPMC that may be underestimated in test systems using L929 cells. GDP-related toxicity appears to be particularly evident in experimental systems using proliferating cells and the milieu of dialysis fluids. Thus, these observations may bear biologic relevance in vivo where HPMC are repeatedly exposed to GDP-containing PDF for extended periods of time.

scholarly journals Involvement of STAT3 Signaling in High Glucose-Induced Epithelial Mesenchymal Transition in Human Peritoneal Mesothelial Cell Line HMrSV5

2019 ◽  
Vol 44 (2) ◽  
pp. 179-187 ◽  
Author(s):  
Pei Zhang ◽  
Hong Dai ◽  
Lei Peng
Keyword(s):  
Cell Line ◽  
High Glucose ◽  
Epithelial Mesenchymal Transition ◽  
Critical Role ◽  
Mesothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mesenchymal Transition ◽  
Stat3 Signaling ◽  
Peritoneal Mesothelial Cell ◽  
Human Peritoneal Mesothelial Cell

Background/Aims: Peritoneal fibrosis (PF) is a common complication in patients receiving long-term peritoneal dialysis, which results in damage to peritoneal functions. Epithelial-mesenchymal transition (EMT) is a key step in the early pathogenesis of PF. Increasing evidence has shown that signal transducer and activator of transcription 3 (STAT3) signaling pathway is involved in EMT and tissue fibrosis by interacting with distinct EMT-inducing molecules, including transforming growth factor (TGF)-β and advanced glycation end products (AGEs). This study investigated the involvement of STAT3 in the PF process. Methods: We used high glucose-treated human peritoneal mesothelial cell line HMrSV5 as an in vitro model to expose the peritoneal mesothelial cells to high-glucose dialysate. Expression of EMT markers was detected by qRT-PCR. Accumulation of methylglyoxal (MGO) and AGEs in the culture supernatant were measured by enzyme-linked immunosorbent assay. Phosphorylation of STAT3 was assessed by Western blot. Results: Results showed that high glucose upregulated TGF-β, increased the productions of MGO and AGEs, and induced EMT in HMrSV5 cells. High glucose also activated the STAT3 pathway. STAT3 inhibitor reduced the high glucose-induced EMT, via reducing TGF-β expression and repressing the accumulation of MGO and AGEs. Conclusion: Our results revealed a critical role for STAT3 signaling in high glucose-induced EMT in HMrSV5 cells, and suggested that inhibition of STAT3 might be a treatment for high glucose-induced fibrogenesis in PF.

scholarly journals Effect of lactate-buffered peritoneal dialysis fluids on human peritoneal mesothelial cell interleukin-6 and prostaglandin synthesis

1995 ◽  
Vol 47 (1) ◽  
pp. 282-293 ◽  
Author(s):  
Janusz Witowski ◽  
Nicholas Topley ◽  
Achim Jörres ◽  
Tomasz Liberek ◽  
Gerald A. Coles ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Interleukin 6 ◽  
Mesothelial Cell ◽  
Prostaglandin Synthesis ◽  
Peritoneal Mesothelial Cell ◽  
Dialysis Fluids ◽  
Human Peritoneal Mesothelial Cell
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