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Acetylcysteine Derivative

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Valérie Verhasselt – One of the best experts on this subject based on the ideXlab platform.

  • N-Acetylcysteine Derivative inhibits CD40-dependent proinflammatory properties of human pancreatic duct cells.
    Pancreas, 2008
    Co-Authors: Olivier Vosters, Claire Beuneu, Michel Goldman, Valérie Verhasselt

    Abstract:

    OBJECTIVES: We recently observed that duct cells constitutively express CD40, a membrane molecule whose engagement results in duct cell activation and proinflammatory cytokine secretion. This observation suggests a potential role of this pathway in the pathogenesis of type 1 diabetes, islet graft rejection, or acute pancreatitis. In this article, we investigated whether a salt Derivative of N-acetyl-L-cysteine, Nacystelyn, could modulate CD40 expression on duct cells and the response of activated duct cells to CD40 engagement. METHODS: We assessed the effects of Nacystelyn on CD40 expression and function in human caucasian pancreatic adenocarcinoma, ATCC n degrees THB-80 (CAPAN-2) cells, a human pancreatic duct cell line. CD40 expression was analyzed by flow cytometry. To assess CAPAN-2 cell responses to CD40 engagement, we looked at nuclear factor-kappaB transcription factor activation using enzyme-linked immunosorbent assay and electrophoretic mobility shift assay and cytokine mRNA levels by quantitative real-time reverse transcriptase polymerase chain reaction. RESULTS: We observed that Nacystelyn dose-dependently inhibited CD40 expression on CAPAN-2 cells as well as CD40-induced nuclear factor kappaB activation and proinflammatory cytokines up-regulation. CONCLUSIONS: Our data suggest that Nacystelyn could be considered as a useful tool to prevent immune and inflammatory responses in pancreatic disorders by interfering with the CD40 pathway in pancreatic duct cells.

  • N-Acetylcysteine Derivative inhibits procoagulant activity of human islet cells
    Diabetologia, 2007
    Co-Authors: Claire Beuneu, Olivier Vosters, Z. Ling, D. Pipeleers, O. Pradier, M. Goldman, Valérie Verhasselt

    Abstract:

    Aims/hypothesis The early loss of beta cells after islet cell transplantation has been attributed in part to blood coagulation at the implant site. Tissue factor expressed by beta cells and contaminating duct cells is considered to activate this process. Here, we investigated the ability of N -acetyl- l -cysteine to suppress the in vitro procoagulant activity of duct cells and human islet cell preparations. Materials and methods The effects of Nacystelyn, a salt Derivative of N -acetyl- l -cysteine, were first assessed on procoagulant activity induced in human plasma by recombinant tissue factor, human primary duct cells or human islet cell preparations. The influence of Nacystelyn on clot formation, platelet counts and d -dimers were measured in a whole blood tubing loop model. Human beta cell viability and insulin synthesis after Nacystelyn treatment were assessed to exclude cytotoxicity of Nacystelyn. Results Nacystelyn efficiently inhibited the procoagulant activity of human recombinant tissue factor, primary duct cells and human islet cell preparations at clinically relevant concentrations without cellular toxicity. Conclusions/interpretation Nacystelyn is a pharmaceutical candidate to reduce early beta cell loss related to tissue factor-dependent coagulation after islet transplantation.

Claire Beuneu – One of the best experts on this subject based on the ideXlab platform.

  • N-Acetylcysteine Derivative inhibits CD40-dependent proinflammatory properties of human pancreatic duct cells.
    Pancreas, 2008
    Co-Authors: Olivier Vosters, Claire Beuneu, Michel Goldman, Valérie Verhasselt

    Abstract:

    OBJECTIVES: We recently observed that duct cells constitutively express CD40, a membrane molecule whose engagement results in duct cell activation and proinflammatory cytokine secretion. This observation suggests a potential role of this pathway in the pathogenesis of type 1 diabetes, islet graft rejection, or acute pancreatitis. In this article, we investigated whether a salt Derivative of N-acetyl-L-cysteine, Nacystelyn, could modulate CD40 expression on duct cells and the response of activated duct cells to CD40 engagement. METHODS: We assessed the effects of Nacystelyn on CD40 expression and function in human caucasian pancreatic adenocarcinoma, ATCC n degrees THB-80 (CAPAN-2) cells, a human pancreatic duct cell line. CD40 expression was analyzed by flow cytometry. To assess CAPAN-2 cell responses to CD40 engagement, we looked at nuclear factor-kappaB transcription factor activation using enzyme-linked immunosorbent assay and electrophoretic mobility shift assay and cytokine mRNA levels by quantitative real-time reverse transcriptase polymerase chain reaction. RESULTS: We observed that Nacystelyn dose-dependently inhibited CD40 expression on CAPAN-2 cells as well as CD40-induced nuclear factor kappaB activation and proinflammatory cytokines up-regulation. CONCLUSIONS: Our data suggest that Nacystelyn could be considered as a useful tool to prevent immune and inflammatory responses in pancreatic disorders by interfering with the CD40 pathway in pancreatic duct cells.

  • N-Acetylcysteine Derivative inhibits procoagulant activity of human islet cells
    Diabetologia, 2007
    Co-Authors: Claire Beuneu, Olivier Vosters, Z. Ling, D. Pipeleers, O. Pradier, M. Goldman, Valérie Verhasselt

    Abstract:

    Aims/hypothesis The early loss of beta cells after islet cell transplantation has been attributed in part to blood coagulation at the implant site. Tissue factor expressed by beta cells and contaminating duct cells is considered to activate this process. Here, we investigated the ability of N -acetyl- l -cysteine to suppress the in vitro procoagulant activity of duct cells and human islet cell preparations. Materials and methods The effects of Nacystelyn, a salt Derivative of N -acetyl- l -cysteine, were first assessed on procoagulant activity induced in human plasma by recombinant tissue factor, human primary duct cells or human islet cell preparations. The influence of Nacystelyn on clot formation, platelet counts and d -dimers were measured in a whole blood tubing loop model. Human beta cell viability and insulin synthesis after Nacystelyn treatment were assessed to exclude cytotoxicity of Nacystelyn. Results Nacystelyn efficiently inhibited the procoagulant activity of human recombinant tissue factor, primary duct cells and human islet cell preparations at clinically relevant concentrations without cellular toxicity. Conclusions/interpretation Nacystelyn is a pharmaceutical candidate to reduce early beta cell loss related to tissue factor-dependent coagulation after islet transplantation.

Olivier Vosters – One of the best experts on this subject based on the ideXlab platform.

  • N-Acetylcysteine Derivative inhibits CD40-dependent proinflammatory properties of human pancreatic duct cells.
    Pancreas, 2008
    Co-Authors: Olivier Vosters, Claire Beuneu, Michel Goldman, Valérie Verhasselt

    Abstract:

    OBJECTIVES: We recently observed that duct cells constitutively express CD40, a membrane molecule whose engagement results in duct cell activation and proinflammatory cytokine secretion. This observation suggests a potential role of this pathway in the pathogenesis of type 1 diabetes, islet graft rejection, or acute pancreatitis. In this article, we investigated whether a salt Derivative of N-acetyl-L-cysteine, Nacystelyn, could modulate CD40 expression on duct cells and the response of activated duct cells to CD40 engagement. METHODS: We assessed the effects of Nacystelyn on CD40 expression and function in human caucasian pancreatic adenocarcinoma, ATCC n degrees THB-80 (CAPAN-2) cells, a human pancreatic duct cell line. CD40 expression was analyzed by flow cytometry. To assess CAPAN-2 cell responses to CD40 engagement, we looked at nuclear factor-kappaB transcription factor activation using enzyme-linked immunosorbent assay and electrophoretic mobility shift assay and cytokine mRNA levels by quantitative real-time reverse transcriptase polymerase chain reaction. RESULTS: We observed that Nacystelyn dose-dependently inhibited CD40 expression on CAPAN-2 cells as well as CD40-induced nuclear factor kappaB activation and proinflammatory cytokines up-regulation. CONCLUSIONS: Our data suggest that Nacystelyn could be considered as a useful tool to prevent immune and inflammatory responses in pancreatic disorders by interfering with the CD40 pathway in pancreatic duct cells.

  • N-Acetylcysteine Derivative inhibits procoagulant activity of human islet cells
    Diabetologia, 2007
    Co-Authors: Claire Beuneu, Olivier Vosters, Z. Ling, D. Pipeleers, O. Pradier, M. Goldman, Valérie Verhasselt

    Abstract:

    Aims/hypothesis The early loss of beta cells after islet cell transplantation has been attributed in part to blood coagulation at the implant site. Tissue factor expressed by beta cells and contaminating duct cells is considered to activate this process. Here, we investigated the ability of N -acetyl- l -cysteine to suppress the in vitro procoagulant activity of duct cells and human islet cell preparations. Materials and methods The effects of Nacystelyn, a salt Derivative of N -acetyl- l -cysteine, were first assessed on procoagulant activity induced in human plasma by recombinant tissue factor, human primary duct cells or human islet cell preparations. The influence of Nacystelyn on clot formation, platelet counts and d -dimers were measured in a whole blood tubing loop model. Human beta cell viability and insulin synthesis after Nacystelyn treatment were assessed to exclude cytotoxicity of Nacystelyn. Results Nacystelyn efficiently inhibited the procoagulant activity of human recombinant tissue factor, primary duct cells and human islet cell preparations at clinically relevant concentrations without cellular toxicity. Conclusions/interpretation Nacystelyn is a pharmaceutical candidate to reduce early beta cell loss related to tissue factor-dependent coagulation after islet transplantation.