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Imene Jaadane - One of the best experts on this subject based on the ideXlab platform.

  • the hidden side of serpinb1 Leukocyte Elastase inhibitor
    Seminars in Cell & Developmental Biology, 2017
    Co-Authors: Alicia Torriglia, Elisabeth Martin, Imene Jaadane
    Abstract:

    SERPINB1, also called Leukocyte Elastase Inhibitor (LEI) is a member of the clade B of SERPINS. It is an intracellular protein and acts primarily to protect the cell from proteases released into the cytoplasm during stress. Its role in inflammation is clear due to its involvement in the resolution of chronic inflammatory lung and bowel diseases. LEI/SERPINB1 intrinsically possesses two enzymatic activities: an antiprotease activity dependent on its reactive site loop, which is analogous to the other proteins of the family and an endonuclease activity which is unveiled by the cleavage of the reactive site loop. The conformational change induced by this cleavage also unveils a bipartite nuclear localization signal allowing the protein to translocate to the nucleus. Recent data indicate that it has also a role in cell migration suggesting that it could be involved in diverse processes like wound healing and malignant metastases.

  • The hidden side of SERPINB1/Leukocyte Elastase Inhibitor.
    Seminars in Cell & Developmental Biology, 2016
    Co-Authors: Alicia Torriglia, Elisabeth Martin, Imene Jaadane
    Abstract:

    SERPINB1, also called Leukocyte Elastase Inhibitor (LEI) is a member of the clade B of SERPINS. It is an intracellular protein and acts primarily to protect the cell from proteases released into the cytoplasm during stress. Its role in inflammation is clear due to its involvement in the resolution of chronic inflammatory lung and bowel diseases. LEI/SERPINB1 intrinsically possesses two enzymatic activities: an antiprotease activity dependent on its reactive site loop, which is analogous to the other proteins of the family and an endonuclease activity which is unveiled by the cleavage of the reactive site loop. The conformational change induced by this cleavage also unveils a bipartite nuclear localization signal allowing the protein to translocate to the nucleus. Recent data indicate that it has also a role in cell migration suggesting that it could be involved in diverse processes like wound healing and malignant metastases.

Alicia Torriglia - One of the best experts on this subject based on the ideXlab platform.

  • the hidden side of serpinb1 Leukocyte Elastase inhibitor
    Seminars in Cell & Developmental Biology, 2017
    Co-Authors: Alicia Torriglia, Elisabeth Martin, Imene Jaadane
    Abstract:

    SERPINB1, also called Leukocyte Elastase Inhibitor (LEI) is a member of the clade B of SERPINS. It is an intracellular protein and acts primarily to protect the cell from proteases released into the cytoplasm during stress. Its role in inflammation is clear due to its involvement in the resolution of chronic inflammatory lung and bowel diseases. LEI/SERPINB1 intrinsically possesses two enzymatic activities: an antiprotease activity dependent on its reactive site loop, which is analogous to the other proteins of the family and an endonuclease activity which is unveiled by the cleavage of the reactive site loop. The conformational change induced by this cleavage also unveils a bipartite nuclear localization signal allowing the protein to translocate to the nucleus. Recent data indicate that it has also a role in cell migration suggesting that it could be involved in diverse processes like wound healing and malignant metastases.

  • The hidden side of SERPINB1/Leukocyte Elastase Inhibitor.
    Seminars in Cell & Developmental Biology, 2016
    Co-Authors: Alicia Torriglia, Elisabeth Martin, Imene Jaadane
    Abstract:

    SERPINB1, also called Leukocyte Elastase Inhibitor (LEI) is a member of the clade B of SERPINS. It is an intracellular protein and acts primarily to protect the cell from proteases released into the cytoplasm during stress. Its role in inflammation is clear due to its involvement in the resolution of chronic inflammatory lung and bowel diseases. LEI/SERPINB1 intrinsically possesses two enzymatic activities: an antiprotease activity dependent on its reactive site loop, which is analogous to the other proteins of the family and an endonuclease activity which is unveiled by the cleavage of the reactive site loop. The conformational change induced by this cleavage also unveils a bipartite nuclear localization signal allowing the protein to translocate to the nucleus. Recent data indicate that it has also a role in cell migration suggesting that it could be involved in diverse processes like wound healing and malignant metastases.

Elisabeth Martin - One of the best experts on this subject based on the ideXlab platform.

  • the hidden side of serpinb1 Leukocyte Elastase inhibitor
    Seminars in Cell & Developmental Biology, 2017
    Co-Authors: Alicia Torriglia, Elisabeth Martin, Imene Jaadane
    Abstract:

    SERPINB1, also called Leukocyte Elastase Inhibitor (LEI) is a member of the clade B of SERPINS. It is an intracellular protein and acts primarily to protect the cell from proteases released into the cytoplasm during stress. Its role in inflammation is clear due to its involvement in the resolution of chronic inflammatory lung and bowel diseases. LEI/SERPINB1 intrinsically possesses two enzymatic activities: an antiprotease activity dependent on its reactive site loop, which is analogous to the other proteins of the family and an endonuclease activity which is unveiled by the cleavage of the reactive site loop. The conformational change induced by this cleavage also unveils a bipartite nuclear localization signal allowing the protein to translocate to the nucleus. Recent data indicate that it has also a role in cell migration suggesting that it could be involved in diverse processes like wound healing and malignant metastases.

  • The hidden side of SERPINB1/Leukocyte Elastase Inhibitor.
    Seminars in Cell & Developmental Biology, 2016
    Co-Authors: Alicia Torriglia, Elisabeth Martin, Imene Jaadane
    Abstract:

    SERPINB1, also called Leukocyte Elastase Inhibitor (LEI) is a member of the clade B of SERPINS. It is an intracellular protein and acts primarily to protect the cell from proteases released into the cytoplasm during stress. Its role in inflammation is clear due to its involvement in the resolution of chronic inflammatory lung and bowel diseases. LEI/SERPINB1 intrinsically possesses two enzymatic activities: an antiprotease activity dependent on its reactive site loop, which is analogous to the other proteins of the family and an endonuclease activity which is unveiled by the cleavage of the reactive site loop. The conformational change induced by this cleavage also unveils a bipartite nuclear localization signal allowing the protein to translocate to the nucleus. Recent data indicate that it has also a role in cell migration suggesting that it could be involved in diverse processes like wound healing and malignant metastases.

Tom Saldeen - One of the best experts on this subject based on the ideXlab platform.

  • Decreased lung hyaluronan in a model of ARDS in the rat: effect of an inhibitor of Leukocyte Elastase.
    Upsala Journal of Medical Sciences, 2012
    Co-Authors: Håkan Sandler, Tom Saldeen
    Abstract:

    BACKGROUND: Hyaluronan (HA) is a component of the extracellular matrix in lung tissue and is normally present at low concentrations in blood. HA is rapidly cleared from blood by the liver. Increased concentrations of plasma HA have been found in patients with acute respiratory distress syndrome (ARDS). We investigated changes in HA levels in plasma, bronchoalveolar lavage fluid (BALF), and lung, and their relationship to pretreatment with a Leukocyte Elastase inhibitor in a rat model of ARDS. METHODS: Rats were randomly assigned to three groups: control, thrombin, and thrombin plus Elastase inhibitor. By use of a radiometric assay, HA was measured in lungs, BALF, and plasma. Tissue samples from the lungs were stained for HA and examined microscopically. Liver circulation and cardiac output were monitored using radiolabeled microspheres. RESULTS: Infusion of thrombin produced a pronounced increase in wet weight to dry weight ratio, and relative lung water content. This increase was blunted by a Leukocyte Elastase inhibitor. A decrease in lung HA and increases in both BALF and plasma HA were found. The Leukocyte Elastase inhibitor counteracted not only the decrease in lung tissue HA, but also the increase in plasma HA. Histologically, there was decreased HA-staining of peribronchial and perivascular areas in the injured rat lung. Decreased liver perfusion was observed after infusion of thrombin. CONCLUSIONS: The decrease in lung HA may be involved in the development of pulmonary edema in this ARDS model, and Leukocyte Elastase may be one cause of this decrease. In addition, an elevated plasma HA level may be an indicator of lung injury.

  • A Leukocyte Elastase inhibitor reduces thrombin-induced pulmonary oedema in the rat: mechanisms of action.
    Pulmonary Pharmacology & Therapeutics, 1998
    Co-Authors: Håkan Sandler, Tom Saldeen
    Abstract:

    Abstract The effect of a selective Leukocyte Elastase inhibitor, ICI 200,355, on thrombin-induced pulmonary oedema was studied in rats. Thrombin administration produced an increase in lung weight ( P P P P P P P P

  • Effect of a synthetic Leukocyte Elastase inhibitor on thrombin-induced pulmonary edema in the rat
    Experimental Lung Research, 1993
    Co-Authors: Håkan Sandler, Mitchell Glass, Tom Saldeen
    Abstract:

    The effect of a synthetic Leukocyte Elastase inhibitor on thrombin-induced pulmonary edema was studied in rats. The chloromethylketone human neutrophil Elastase inhibitor, ICI 200,355, blunted rat Leukocyte Elastase activity in rat lung tissue. Administration of thrombin produced a significant increase (p < .01) in lung weight. The wet weight to dry weight ratio (WW/DW) and relative water contents were also significantly elevated (p < .01). Pretreatment with ICI 200,355 (200 μg/kg h−1) resulted in significant reductions (p < .05) in lung weight and a tendency to decrease WW/DW and water content compared with animals given thrombin alone. It is possible that the Elastase inhibitor effectively reduced the rate of thrombin-induced pulmonary edema by attenuation of increased vascular permeability.

Håkan Sandler - One of the best experts on this subject based on the ideXlab platform.

  • Decreased lung hyaluronan in a model of ARDS in the rat: effect of an inhibitor of Leukocyte Elastase.
    Upsala Journal of Medical Sciences, 2012
    Co-Authors: Håkan Sandler, Tom Saldeen
    Abstract:

    BACKGROUND: Hyaluronan (HA) is a component of the extracellular matrix in lung tissue and is normally present at low concentrations in blood. HA is rapidly cleared from blood by the liver. Increased concentrations of plasma HA have been found in patients with acute respiratory distress syndrome (ARDS). We investigated changes in HA levels in plasma, bronchoalveolar lavage fluid (BALF), and lung, and their relationship to pretreatment with a Leukocyte Elastase inhibitor in a rat model of ARDS. METHODS: Rats were randomly assigned to three groups: control, thrombin, and thrombin plus Elastase inhibitor. By use of a radiometric assay, HA was measured in lungs, BALF, and plasma. Tissue samples from the lungs were stained for HA and examined microscopically. Liver circulation and cardiac output were monitored using radiolabeled microspheres. RESULTS: Infusion of thrombin produced a pronounced increase in wet weight to dry weight ratio, and relative lung water content. This increase was blunted by a Leukocyte Elastase inhibitor. A decrease in lung HA and increases in both BALF and plasma HA were found. The Leukocyte Elastase inhibitor counteracted not only the decrease in lung tissue HA, but also the increase in plasma HA. Histologically, there was decreased HA-staining of peribronchial and perivascular areas in the injured rat lung. Decreased liver perfusion was observed after infusion of thrombin. CONCLUSIONS: The decrease in lung HA may be involved in the development of pulmonary edema in this ARDS model, and Leukocyte Elastase may be one cause of this decrease. In addition, an elevated plasma HA level may be an indicator of lung injury.

  • A Leukocyte Elastase inhibitor reduces thrombin-induced pulmonary oedema in the rat: mechanisms of action.
    Pulmonary Pharmacology & Therapeutics, 1998
    Co-Authors: Håkan Sandler, Tom Saldeen
    Abstract:

    Abstract The effect of a selective Leukocyte Elastase inhibitor, ICI 200,355, on thrombin-induced pulmonary oedema was studied in rats. Thrombin administration produced an increase in lung weight ( P P P P P P P P

  • Effect of a synthetic Leukocyte Elastase inhibitor on thrombin-induced pulmonary edema in the rat
    Experimental Lung Research, 1993
    Co-Authors: Håkan Sandler, Mitchell Glass, Tom Saldeen
    Abstract:

    The effect of a synthetic Leukocyte Elastase inhibitor on thrombin-induced pulmonary edema was studied in rats. The chloromethylketone human neutrophil Elastase inhibitor, ICI 200,355, blunted rat Leukocyte Elastase activity in rat lung tissue. Administration of thrombin produced a significant increase (p < .01) in lung weight. The wet weight to dry weight ratio (WW/DW) and relative water contents were also significantly elevated (p < .01). Pretreatment with ICI 200,355 (200 μg/kg h−1) resulted in significant reductions (p < .05) in lung weight and a tendency to decrease WW/DW and water content compared with animals given thrombin alone. It is possible that the Elastase inhibitor effectively reduced the rate of thrombin-induced pulmonary edema by attenuation of increased vascular permeability.