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  • Stress responses and conditioning effects in mesothelial cells exposed to peritoneal dialysis fluid. 19231869

    Renal replacement therapy by peritoneal dialysis is frequently complicated by technical failure. Peritoneal dialysis fluids (PDF) cause injury to the peritoneal mesothelial cell layer due to their cytotoxicity. As only isolated elements of the involved cellular processes have been studied before, we aimed at a global assessment of the mesothelial stress response to PDF. Following single or repeated exposure to PDF or control medium, proteomics and bioinformatics techniques were combined to study effects in mesothelial cells (MeT-5A). Protein expression was assessed by two-dimensional gel electrophoresis, and significantly altered spots were identified by MALDI-TOF MS and MS2 techniques. The lists of experimentally derived candidate proteins were expanded by a next neighbor approach and analyzed for significantly enriched biological processes. To address the problem of an unknown portion of false positive spots in 2DGE, only proteins showing significant p-values on both levels were further interpreted. Single PDF exposure resulted in reduction of biological processes in favor of reparative responses, including protein metabolism, modification and folding, with chaperones as a major subgroup. The observed biological processes triggered by this acute PDF exposure mainly contained functionally interwoven multitasking proteins contributing as well to cytoskeletal reorganization and defense mechanisms. Repeated PDF exposure resulted in attenuated protein regulation, reflecting inhibition of stress responses by high levels of preinduced chaperones. The identified proteins were less attributable to acute cellular injury but rather to specialized functions with a reduced number of involved multitasking proteins. This finding agrees well with the concept of conditioning effects and cytoprotection. In conclusion, this study describes the reprogrammed proteome of mesothelial cells during recovery from PDF exposure and adaption to repetitive stress. A broad stress response with a number of highly overlapping processes and multitasking proteins shifts toward a more specific response of only few less overlapping processes.
    Document Type:
    Reference
    Product Catalog Number:
    AB3563

  • Evidence for HSP-mediated cytoskeletal stabilization in mesothelial cells during acute experimental peritoneal dialysis. 17210795

    Low biocompatibility of peritoneal dialysis fluid (PDF) injures mesothelial cells and activates their stress response. In this study, we investigated the role of heat shock proteins (HSP), the main cytoprotective effectors of the stress response, in cytoskeletal stabilization of mesothelial cells in experimental peritoneal dialysis. In cultured human mesothelial cells, cytoskeletal integrity was assessed by detergent extractability of marker proteins following in vitro PDF exposure. Effects of HSP on stabilization of ezrin were evaluated by a conditioning protocol (PDF pretreatment) and repair assay, based on coincubation of cytoskeletal protein fractions with recombinant HSP-72 or HSP-72 antibodies. In the rat model, detachment of mesothelial cells from their peritoneal monolayer during in vivo PDF exposure was assessed with and without overexpression of HSP-72 (by heat conditioning). In vitro, cytoskeletal disruption on sublethal PDF exposure was demonstrated by significantly altered detergent extractability of ezrin and ZO-1. Restoration was associated with significant induction and cytoskeletal redistribution of HSP during recovery. Both the conditioning protocol and in vitro repair assay provided evidence for HSP-72-mediated cytoskeletal stabilization. In the rat model, overexpression of HSP-72 following heat conditioning resulted in significantly reduced detachment of mesothelial cells on in vivo exposure to PDF. Our results establish an essential role of HSP in repair and cytoprotection of cytoskeletal integrity in mesothelial cells following acute in vitro and in vivo exposure to PDF. Repeated exposure to PDF, as is the rule in the clinical setting, may not only cause repeat injury to mesothelial cells but rather represents a kind of inadvertent conditioning treatment.
    Document Type:
    Reference
    Product Catalog Number:
    05-369
    Product Catalog Name:
    Anti-Na+/K+ ATPase α-1 Antibody, clone C464.6

  • Sclerostin serum levels correlate positively with bone mineral density and microarchitecture in haemodialysis patients. 21613383

    Sclerostin is a soluble inhibitor of osteoblast function. Sclerostin is downregulated by the parathyroid hormone (PTH). Here, it was investigated whether sclerostin levels are influenced by intact (i) PTH and whether sclerostin is associated with bone turnover, microarchitecture and mass in dialysis patients.
    Document Type:
    Reference
    Product Catalog Number:
    MAB1406
    Product Catalog Name:
    Anti-Thy-1.1 Antibody, clone OX-7

  • Oxidative stress-associated shape transformation and Membrane proteome remodeling in erythrocytes of end stage renal disease patients on hemodialysis. 21515423

    This study was designed to evaluate the oxidative stress status of erythrocytes and its association with cellular ultrastructure and membrane proteome modifications in patients with end stage renal disease (ESRD) on hemodialysis (HD). For that purpose, we studied red blood cells\' (RBCs) modifications in twelve non-diabetic ESRD patients that were responsive in erythropoietin therapy. Intracellular ROS levels were measured by fluorometry, RBCs ultra-structure was examined by electron microscopy, while the membrane proteome by electrophoresis and immunoblotting. Compared to the healthy subjects, the uremic RBCs exhibited significantly increased ROS accumulation. Dialysis partially ameliorated the basal ROS levels but triggered cellular sensitivity to exogenous oxidative stimuli. Common membrane modifications involved loss, aggregation, fragmentation and carbonylation of critical components as well as over-expression of stress markers. HD significantly contributed to membrane proteome remodeling, especially for aquaporin-1, peroxiredoxin-2 and ubiquitinated proteins. The intracellular redox status and the closely associated membrane modifications seemed to be related to membrane instability, loss of surface area through vesiculation, echinocytosis and stomatocytosis. Our data evinced a network of interactions among the uremic toxins, the RBCs membrane composition and the cellular shape modifications in ESRD, which is developed around a core of oxidative provocations and cellular responses.Copyright © 2011 Elsevier B.V. All rights reserved.
    Document Type:
    Reference
    Product Catalog Number:
    S7150
    Product Catalog Name:
    OxyBlot Protein Oxidation Detection Kit

  • Epigallocatechin gallate suppresses peritoneal fibrosis in mice. 22101032

    Long-term peritoneal dialysis (PD) leads to histological changes in the peritoneal membrane. Angiogenesis and inflammation caused by glucose degradation products (GDPs) play crucial roles in peritoneal fibrosis. One such GDP is methylglyoxal (MGO), which enhances the formation of advanced glycation end products (AGEs). AGEs bind to their receptor (RAGE) and activate nuclear factor-?B (NF-?B), which is a key regulator of angiogenesis and inflammation. Recent studies have indicated that (-)-epigallocatechin gallate (EGCG), a tea polyphenol, inhibits angiogenesis and inflammation. Here, we examined whether EGCG suppresses peritoneal fibrosis in mice. Based on preliminary examination, 2mL of 40mM MGO or PD fluid was injected intraperitoneally and EGCG (50mg/kg) or saline was injected subcutaneously for 3weeks. In comparison to PD fluid+saline-treated mice, the peritoneal tissues of MGO+saline-treated mice showed marked thickening of the submesothelial compact zone. In the submesothelial compact zone of the MGO+saline-treated mice, CD31-positive vessels and vascular endothelial growth factor-positive cells were significantly increased, as were inflammation, F4/80-positive macrophages, and monocyte chemotactic protein-1. Moreover, 8-hydroxydeoxyguanosine, a marker of reactive oxygen species, and NF-?B, determined by Southwestern histochemistry, in the submesothelial compact zone were also increased in MGO+saline-treated mice. These changes were attenuated in MGO+EGCG-treated mice. We demonstrated that EGCG treatment suppresses peritoneal fibrosis via inhibition of NF-?B. Furthermore, EGCG inhibits reactive oxygen species production. The results of this study indicate that EGCG is a potentially novel candidate for the treatment of peritoneal fibrosis.
    Document Type:
    Reference
    Product Catalog Number:
    AB5484

  • Mizoribine suppresses the progression of experimental peritoneal fibrosis in a rat model. 19390220

    BACKGROUND/AIMS: Peritoneal fibrosis is a serious complication of peritoneal dialysis (PD). It has been reported that administration of mizoribine, an effective immunosuppressant, ameliorated renal fibrosis in a rat model of unilateral ureteral obstruction. We therefore examined the effects of mizoribine in an experimental model of peritoneal fibrosis. METHODS: 24 rats were given a daily intraperitoneal injection of chlorhexidine gluconate and ethanol dissolved in saline. The rats were divided into three groups (n = 8 per group) that received either vehicle or mizoribine at a dose of 2 or 8 mg/kg once a day. 28 days after the start of the treatments the rats were sacrificed and peritoneal tissue samples collected. Macrophage infiltration (ED1), myofibroblast accumulation (alpha-smooth muscle actin (SMA)) and expression of type III collagen, transforming growth factor (TGF)-beta and monocyte chemotactic protein-1 (MCP-1) were examined by immunohistochemistry. RESULTS: Mizoribine significantly suppressed submesothelial zone thickening and reduced macrophage infiltration. Mizoribine also reduced collagen III(+) area and decreased the number of alpha-SMA(+), TGF-beta(+) and MCP-1(+) cells. The magnitude of the changes observed was dose-dependent. CONCLUSION: The administration of mizoribine prevented the progression of peritoneal fibrosis in this rat model. Mizoribine may represent a novel therapy for peritoneal sclerosis in patients undergoing long-term PD.
    Document Type:
    Reference
    Product Catalog Number:
    AB757P
    Product Catalog Name:
    Anti-Collagen Type III Antibody

  • Evaluation of two treatments in superovulation of mares. 10732063

    The efficiency of superovulating mares with an enriched fraction of equine follicle-stimulating hormone (feFSH) and an equine pituitary extract (EPE) with similar FSH content but differing in the LH amount was compared. Mares were randomly assigned to an feFSH (n = 5) or EPE (n = 5) treatment. The experimental period was of 2 successive estrous cycles, with the first cycle as the control. At Days 6 and 7 of the estrous cycle, the mares received 250 micrograms i.m. cloprostenol. The treatments consisted of daily injections of 25 mg feFSH or EPE beginning on Day 6 post ovulation. Mares were inseminated every other day until the last ovulation was detected. When the mares in the control and treatment cycles developed at least 1 or 2 > or = 35-mm follicle, respectively, the treatment was interrupted, and a single injection of EPE (25 mg, i.v.) was administered to induce ovulation(s). Nonsurgical embryo recovery was performed 6 or 7 d after ovulation in both control and treatment cycles. The number of ovulations per mare was not significantly different (P > 0.05) between feFSH and EPE groups, but both were higher (P < 0.05) than that of the control cycle. The number of recovered embryos per ovulation was similar (P > 0.05) for control, feFSH and EPE groups. The high amount of LH presented in EPE did not affect the superovulatory response of the mares. Superovulatory treatments increased the ovulation rate of mares but did not affect the embryo recovery rate per ovulation.
    Document Type:
    Reference
    Product Catalog Number:
    16-103
    Product Catalog Name:
    Anti-Phosphotyrosine Antibody, clone 4G10®, Biotin Conjugate

  • Endostatin peptide, an inhibitor of angiogenesis, prevents the progression of peritoneal sclerosis in a mouse experimental model. 17191085

    Peritoneal sclerosis is a major and serious complication in patients on long-term continuous ambulatory peritoneal dialysis (PD). The involvement of angiogenesis and proangiogenic factors such as vascular endothelial growth factor (VEGF)-A in progressing peritoneal sclerosis has been reported. We previously reported the therapeutic efficacy of endostatin peptide, a potent inhibitor of angiogenesis derived from type XVIII collagen, in a mouse diabetic nephropathy model. Here, we examined the therapeutic effect of endostatin peptide in preventing progression in a mouse peritoneal sclerosis model. Male ICR mice received intraperitoneal injections of chlorhexidine gluconate (CG) every other day to induce peritoneal sclerosis. Endostatin peptide (1 or 4 mg/kg/day) was administered via subcutaneously implanted osmotic minipumps. Peritoneal sclerosis (day 24) was significantly suppressed by endostatin peptide in a dose-dependent manner. Peritoneal accumulation of type III collagen was significantly suppressed by endostatin peptide. Increase in the number of CD31(+) blood vessels, F4/80(+) monocyte/macrophage accumulation, and 5-bromodeoxyuridine(+) proliferating cells was significantly inhibited by endostatin peptide. Increase in peritoneal expression of VEGF-A, profibrotic transforming growth factor-beta1, and alpha-smooth muscle actin was suppressed by endostatin peptide. Immunoreactivity for endogenous endostatin (whole molecule) and endostatin receptor alpha5beta1-integrin was increased and colocalized to CD31(+) blood vessels in the thickened peritonea of CG-injected mice. These results demonstrate the potential use of antiangiogenic endostatin peptide as a novel therapeutic agent in preventing peritoneal sclerosis, a severe complication in patients undergoing long-term PD.
    Document Type:
    Reference
    Product Catalog Number:
    MAB1398Z
    Product Catalog Name:
    Anti-PECAM-1 Antibody, clone 2H8, Azide Free