Arachidonic acid metabolism by cultured mesothelial cells

Coene, M.‐C.; Hove, C. Van; Claeys, Magda; Herman, Arnold G.

doi:10.1016/0005-2760(82)90127-8

Cited by 49 publications

(4 citation statements)

References 13 publications

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“…The basic concepts of intraperito neal chemotherapy developed from peritoneal dialysis studies, many of which yielded new insight into the func tion of human peritoneal mésothélial cells (HPMC). It has been demonstrated that a monolayer of mésothélial cells not only lines the peritoneal cavity and forms an active permeability barrier regulating the passage of fluid and solutes across the peritoneal membrane [4] but also due to its significant biosynthetic capacity is a major source of peritoneal phospholipids [5], prostaglandins [6] and cyto kines [7,8], During peritoneal dialysis HPMC are continually ex posed to a nonphysiological environment of the dialysis solution. In this respect previous studies of peritoneal biopsy material from patients on chronic peritoneal dialy sis have revealed many alterations in mesothelial cell morphology including loss of the surface microvilli, dis-ruption of the intercellular junctions, and detachment from the subjacent tissue [9], It has also been shown that unused dialysis fluids significantly reduce HPMC viabili ty in vitro [10].…”

Section: Introductionmentioning

confidence: 99%

Effect of Methotrexate, Doxorubicin and Mitoxantrone on Human Peritoneal Mesothelial Cell Function in vitro

1995

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Recent studies have demonstrated that intraperitoneal instillation of dialysis solutions and drug additives may adversely affect the function of peritoneal cell populations. Therefore the aim of the present investigation was to examine the short-term effects of antineoplastic agents on human peritoneal mesothelial cells (HPMC). We have assessed the integrity of HPMC membrane and mechanisms of intracellular potassium transport. There was no evidence of significant cytotoxicity (as measured by ⁸⁶Rb release) during a 60-min exposure of HPMC to either methotrexate (10^-6-10^-4M), doxorubicin (10^-7-10^-5M) or mitoxantrone (10^-7-10^-5 M). In HPMC exposed to doxorubicin (10^-6M) the intracellular transport of potassium, as assessed with ⁸⁶Rb as its analogue, was not affected. Methotrexate (10^-5M) diminished Na, K-ATPase activity and simultaneously enhanced the ⁸⁶Rb transport via furosemide-sensitive pathway. Mitoxantrone reduced the furosemide-sensitive ⁸⁶Rb influx in a dose-dependent manner and at a concentration of 10^-4M it also impaired the ouabain-dependent ⁸⁶Rb influx. These data demonstrate that antineoplastic agents interfere with HPMC function which might contribute to the onco-static-induced peritoneal toxicity.

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Section: Introductionmentioning

confidence: 99%

Effect of Methotrexate, Doxorubicin and Mitoxantrone on Human Peritoneal Mesothelial Cell Function in vitro

1995

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“…Mesothelial cells play important roles in both peritoneal transport functions and remodeling, the latter through its controlled synthesis of cytokines, chemokines, growth factors, prostaglandins, and matrix proteins (1)(2)(3)(4). Injury to the mesothelium represents an important initiating step, leading to the progressive histologic changes of the peritoneum in peritoneal dialysis (PD).…”

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confidence: 99%

Reduction of Perlecan Synthesis and Induction of TGF-β1 in Human Peritoneal Mesothelial Cells Due to High Dialysate Glucose Concentration

Yung¹,

Chen²,

Tsang³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Prolonged exposure of the peritoneal mesothelium to high dialysate glucose concentrations reduces anionic sites that are critical to its selective permeability, thereby impairing the peritoneal transport properties in patients on long-term peritoneal dialysis (PD). Perlecan, an anionic heparan sulfate proteoglycan, is pivotal to the selective permeability of basement membranes, and high glucose concentrations modulate its synthesis in mesangial cells. The effect of glucose on perlecan expression in the peritoneal mesothelium has not been established. We investigated perlecan expression in peritoneal biopsies from patients on PD, and the effect of high glucose concentrations on perlecan synthesis in cultured human peritoneal mesothelial cells (HPMC). Peritoneal biopsies from PD patients showed reduced perlecan expression compared with controls. Exposure of HPMC to high glucose concentrations resulted in a dose-dependent reduction in the synthesis of perlecan polypeptide and its deposition into the extracellular matrix. These effects were mediated in part through the induction of TGF-␤1. Characterization studies showed that perlecan synthesized by HPMC contained solely heparan sulfate glycosaminoglycan (HS GAG) chains, and [35 S]-incorporation studies demonstrated progressive reduction of their de novo synthesis with increasing glucose concentrations (68142 Ϯ 3658, 48147 Ϯ 2517, 31468 Ϯ 5781, and 25575 Ϯ 3621 cpm/g cellular protein for 5 mM, 30 mM, 75 mM, and 120 mM D-glucose, respectively; P Ͻ 0.001 for 5 mM versus 30 mM D-glucose, and P Ͻ 0.0001 for 5 mM versus 75 mM or 120 mM D-glucose). Both the length and the charge density of the HS GAG chains remained unchanged. Reduction of peritoneal perlecan expression in long-term PD was attributed to high dialysate glucose concentrations, which induced TGF-␤1 and reduced perlecan synthesis in HPMC. Since perlecan can sequester growth factors, thereby modulating cell migration and differentiation perturbation of peritoneal perlecan expression contributes to the structural and functional changes of the peritoneum in long-term PD.

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“…2 A). At 6 h, the total number of neutrophils recovered from the pleural spaces exposed to TNF was more than threefold greater than that from the opposite side (Table I). There was no increase in the entry of radiolabeled protein.…”

Section: Resultsmentioning

confidence: 93%

“…Although previously considered a passive lining cell, pleural mesothelial cells exhibit a variety of functions that suggest that they play a role in the pathogenesis of inflammation. For example, mesothelial cells have been shown to phagocytose particles including asbestos fibers (5), produce prostaglandins in response to nonspecific irritants (6), and express immune-associated antigens in response to interferon-^y (7). In a recent report by Antony et al (8), rabbit pleural mesothelial cells were shown to produce a neutrophil chemotaxin, a 6-9-kD peptide.…”

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confidence: 99%

Evidence of a role for mesothelial cell-derived interleukin 8 in the pathogenesis of asbestos-induced pleurisy in rabbits.

Boylan¹,

Rüegg²,

Kim³

et al. 1992

J. Clin. Invest.

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IntroductionAlthough acute asbestos-induced pleurisy is characterized by an influx of neutrophils, the identity of the factors that attract these cells to the pleural space and the source of the factors are unknown. We found that instillation of crocidolite asbestos into the pleural space of rabbits led to the appearance in pleural liquid of chemotactic activity for neutrophils, and that this chemotactic activity was inhibited significantly by a neutralizing antibody to human interleukin 8 (IL-8). Cultured rabbit pleural mesothelial cells incubated with crocidolite asbestos also released chemotactic activity for neutrophils, which was inhibited significantly by the anti-IL-8 antibody. To determine whether rabbit pleural mesothelial cells synthesize IL-8, we generated a probe for rabbit IL-8 mRNA by amplifying cDNA prepared from stimulated pleural mesothelial cells using the polymerase chain reaction (PCR) and primers based on homologous sequences in human and sheep IL-8 cDNAs. Homology-based PCR yielded a single cDNA fragment with a nucleotide sequence 88% identical to that of a corresponding region of human IL-8 cDNA. With the radiolabeled PCR product as a probe, we demonstrated rapid induction of IL-8 mRNA expression in pleural mesothelial cells exposed to asbestos. As expected, tumor necrosis factor-a also led to the appearance of IL-8 in the rabbit pleural space and stimulated cultured pleural mesothelial cells to synthesize and release IL-8.

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Arachidonic acid metabolism by cultured mesothelial cells

Cited by 49 publications

References 13 publications

Effect of Methotrexate, Doxorubicin and Mitoxantrone on Human Peritoneal Mesothelial Cell Function in vitro

Effect of Methotrexate, Doxorubicin and Mitoxantrone on Human Peritoneal Mesothelial Cell Function in vitro

Reduction of Perlecan Synthesis and Induction of TGF-β1 in Human Peritoneal Mesothelial Cells Due to High Dialysate Glucose Concentration

Evidence of a role for mesothelial cell-derived interleukin 8 in the pathogenesis of asbestos-induced pleurisy in rabbits.

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