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Cn Serhan - One of the best experts on this subject based on the ideXlab platform.

  • new maresin conjugates in tissue regeneration pathway counters Leukotriene D4 stimulated vascular responses
    The FASEB Journal, 2018
    Co-Authors: Nan Chiang, Bw Spur, Ian R Riley, Jesmond Dalli, Ana R Rodriguez, Cn Serhan
    Abstract:

    Resolution of acute inflammation is governed, in part, by lipid mediator class switching from proinflammatory eicosanoids to specialized proresolving mediators, including a recently identified new pathway of mediators, termed maresin conjugates in tissue regeneration (MCTR), which includes MCTR1, MCTR2, and MCTR3. Here, we addressed whether each MCTR can impact the known vascular actions of cysteinyl Leukotrienes. Leukotriene D4 (LTD4; 1.5 nmol/mouse) initiated vascular leakage in mouse cremaster vessels, which was reduced (>75%) by MCTR1 and MCTR2 (0.15 nmol each). With isolated Ciona intestinalis (sea squirt) primordial hearts, LTD4 (1-100 nM) induced negative inotropic action and lowered heartbeats 20-30%. Each MCTR (1-100 nM) prevented LTD4-reduced heart rates. With human cysteinyl Leukotriene receptor-1 (CysLT1) expressed in CHO cells, each MCTR (10-100 nM) significantly reduced LTD4-initiated signaling. To assess the contribution of CysLT1 in the proresolving actions of MCTR, we carried out human macrophage (MΦ) phagocytosis. Each MCTR (0.1-10 nM) stimulated human MΦ phagocytosis of live Escherichia coli, whereas LTD4 did not stimulate phagocytosis. MCTR-activated phagocytosis was significantly blocked by a pharmacologic receptor antagonist (MK571). With both CHO-CysLT1 and human MΦs, each MCTR competed for specific [3H]-LTD4 binding with apparent lower affinity than LTD4. Thus, each MCTR functionally interacts with human CysLT1 to pharmacologically counter-regulate vascular responses and stimulate physiologic phagocytosis with MΦs.-Chiang, N., Riley, I. R., Dalli, J., Rodriguez, A. R., Spur, B. W., Serhan, C. N. New maresin conjugates in tissue regeneration pathway counters Leukotriene D4-stimulated vascular responses.

  • New maresin conjugates in tissue regeneration pathway counters Leukotriene D4-stimulated vascular responses.
    'FASEB', 2018
    Co-Authors: Chiang N, Dalli J, Ir Riley, Ar Rodriguez, Bw Spur, Cn Serhan
    Abstract:

    Resolution of acute inflammation is governed, in part, by lipid mediator class switching from proinflammatory eicosanoids to specialized proresolving mediators, including a recently identified new pathway of mediators, termed maresin conjugates in tissue regeneration (MCTR), which includes MCTR1, MCTR2, and MCTR3. Here, we addressed whether each MCTR can impact the known vascular actions of cysteinyl Leukotrienes. Leukotriene D4 (LTD4; 1.5 nmol/mouse) initiated vascular leakage in mouse cremaster vessels, which was reduced (>75%) by MCTR1 and MCTR2 (0.15 nmol each). With isolated Ciona intestinalis (sea squirt) primordial hearts, LTD4 (1-100 nM) induced negative inotropic action and lowered heartbeats 20-30%. Each MCTR (1-100 nM) prevented LTD4-reduced heart rates. With human cysteinyl Leukotriene receptor-1 (CysLT1) expressed in CHO cells, each MCTR (10-100 nM) significantly reduced LTD4-initiated signaling. To assess the contribution of CysLT1 in the proresolving actions of MCTR, we carried out human macrophage (MΦ) phagocytosis. Each MCTR (0.1-10 nM) stimulated human MΦ phagocytosis of live Escherichia coli, whereas LTD4 did not stimulate phagocytosis. MCTR-activated phagocytosis was significantly blocked by a pharmacologic receptor antagonist (MK571). With both CHO-CysLT1 and human MΦs, each MCTR competed for specific [3H]-LTD4 binding with apparent lower affinity than LTD4. Thus, each MCTR functionally interacts with human CysLT1 to pharmacologically counter-regulate vascular responses and stimulate physiologic phagocytosis with MΦs.-Chiang, N., Riley, I. R., Dalli, J., Rodriguez, A. R., Spur, B. W., Serhan, C. N. New maresin conjugates in tissue regeneration pathway counters Leukotriene D4-stimulated vascular responses.This work was supported, in part, by U.S. National Institutes of Health, National Institute of General Medical Sciences Grants P01-GM095467 and R01-GM38765 (to C.N.S.

Bw Spur - One of the best experts on this subject based on the ideXlab platform.

  • new maresin conjugates in tissue regeneration pathway counters Leukotriene D4 stimulated vascular responses
    The FASEB Journal, 2018
    Co-Authors: Nan Chiang, Bw Spur, Ian R Riley, Jesmond Dalli, Ana R Rodriguez, Cn Serhan
    Abstract:

    Resolution of acute inflammation is governed, in part, by lipid mediator class switching from proinflammatory eicosanoids to specialized proresolving mediators, including a recently identified new pathway of mediators, termed maresin conjugates in tissue regeneration (MCTR), which includes MCTR1, MCTR2, and MCTR3. Here, we addressed whether each MCTR can impact the known vascular actions of cysteinyl Leukotrienes. Leukotriene D4 (LTD4; 1.5 nmol/mouse) initiated vascular leakage in mouse cremaster vessels, which was reduced (>75%) by MCTR1 and MCTR2 (0.15 nmol each). With isolated Ciona intestinalis (sea squirt) primordial hearts, LTD4 (1-100 nM) induced negative inotropic action and lowered heartbeats 20-30%. Each MCTR (1-100 nM) prevented LTD4-reduced heart rates. With human cysteinyl Leukotriene receptor-1 (CysLT1) expressed in CHO cells, each MCTR (10-100 nM) significantly reduced LTD4-initiated signaling. To assess the contribution of CysLT1 in the proresolving actions of MCTR, we carried out human macrophage (MΦ) phagocytosis. Each MCTR (0.1-10 nM) stimulated human MΦ phagocytosis of live Escherichia coli, whereas LTD4 did not stimulate phagocytosis. MCTR-activated phagocytosis was significantly blocked by a pharmacologic receptor antagonist (MK571). With both CHO-CysLT1 and human MΦs, each MCTR competed for specific [3H]-LTD4 binding with apparent lower affinity than LTD4. Thus, each MCTR functionally interacts with human CysLT1 to pharmacologically counter-regulate vascular responses and stimulate physiologic phagocytosis with MΦs.-Chiang, N., Riley, I. R., Dalli, J., Rodriguez, A. R., Spur, B. W., Serhan, C. N. New maresin conjugates in tissue regeneration pathway counters Leukotriene D4-stimulated vascular responses.

  • New maresin conjugates in tissue regeneration pathway counters Leukotriene D4-stimulated vascular responses.
    'FASEB', 2018
    Co-Authors: Chiang N, Dalli J, Ir Riley, Ar Rodriguez, Bw Spur, Cn Serhan
    Abstract:

    Resolution of acute inflammation is governed, in part, by lipid mediator class switching from proinflammatory eicosanoids to specialized proresolving mediators, including a recently identified new pathway of mediators, termed maresin conjugates in tissue regeneration (MCTR), which includes MCTR1, MCTR2, and MCTR3. Here, we addressed whether each MCTR can impact the known vascular actions of cysteinyl Leukotrienes. Leukotriene D4 (LTD4; 1.5 nmol/mouse) initiated vascular leakage in mouse cremaster vessels, which was reduced (>75%) by MCTR1 and MCTR2 (0.15 nmol each). With isolated Ciona intestinalis (sea squirt) primordial hearts, LTD4 (1-100 nM) induced negative inotropic action and lowered heartbeats 20-30%. Each MCTR (1-100 nM) prevented LTD4-reduced heart rates. With human cysteinyl Leukotriene receptor-1 (CysLT1) expressed in CHO cells, each MCTR (10-100 nM) significantly reduced LTD4-initiated signaling. To assess the contribution of CysLT1 in the proresolving actions of MCTR, we carried out human macrophage (MΦ) phagocytosis. Each MCTR (0.1-10 nM) stimulated human MΦ phagocytosis of live Escherichia coli, whereas LTD4 did not stimulate phagocytosis. MCTR-activated phagocytosis was significantly blocked by a pharmacologic receptor antagonist (MK571). With both CHO-CysLT1 and human MΦs, each MCTR competed for specific [3H]-LTD4 binding with apparent lower affinity than LTD4. Thus, each MCTR functionally interacts with human CysLT1 to pharmacologically counter-regulate vascular responses and stimulate physiologic phagocytosis with MΦs.-Chiang, N., Riley, I. R., Dalli, J., Rodriguez, A. R., Spur, B. W., Serhan, C. N. New maresin conjugates in tissue regeneration pathway counters Leukotriene D4-stimulated vascular responses.This work was supported, in part, by U.S. National Institutes of Health, National Institute of General Medical Sciences Grants P01-GM095467 and R01-GM38765 (to C.N.S.

Nan Chiang - One of the best experts on this subject based on the ideXlab platform.

  • new maresin conjugates in tissue regeneration pathway counters Leukotriene D4 stimulated vascular responses
    The FASEB Journal, 2018
    Co-Authors: Nan Chiang, Bw Spur, Ian R Riley, Jesmond Dalli, Ana R Rodriguez, Cn Serhan
    Abstract:

    Resolution of acute inflammation is governed, in part, by lipid mediator class switching from proinflammatory eicosanoids to specialized proresolving mediators, including a recently identified new pathway of mediators, termed maresin conjugates in tissue regeneration (MCTR), which includes MCTR1, MCTR2, and MCTR3. Here, we addressed whether each MCTR can impact the known vascular actions of cysteinyl Leukotrienes. Leukotriene D4 (LTD4; 1.5 nmol/mouse) initiated vascular leakage in mouse cremaster vessels, which was reduced (>75%) by MCTR1 and MCTR2 (0.15 nmol each). With isolated Ciona intestinalis (sea squirt) primordial hearts, LTD4 (1-100 nM) induced negative inotropic action and lowered heartbeats 20-30%. Each MCTR (1-100 nM) prevented LTD4-reduced heart rates. With human cysteinyl Leukotriene receptor-1 (CysLT1) expressed in CHO cells, each MCTR (10-100 nM) significantly reduced LTD4-initiated signaling. To assess the contribution of CysLT1 in the proresolving actions of MCTR, we carried out human macrophage (MΦ) phagocytosis. Each MCTR (0.1-10 nM) stimulated human MΦ phagocytosis of live Escherichia coli, whereas LTD4 did not stimulate phagocytosis. MCTR-activated phagocytosis was significantly blocked by a pharmacologic receptor antagonist (MK571). With both CHO-CysLT1 and human MΦs, each MCTR competed for specific [3H]-LTD4 binding with apparent lower affinity than LTD4. Thus, each MCTR functionally interacts with human CysLT1 to pharmacologically counter-regulate vascular responses and stimulate physiologic phagocytosis with MΦs.-Chiang, N., Riley, I. R., Dalli, J., Rodriguez, A. R., Spur, B. W., Serhan, C. N. New maresin conjugates in tissue regeneration pathway counters Leukotriene D4-stimulated vascular responses.

Chiang N - One of the best experts on this subject based on the ideXlab platform.

  • New maresin conjugates in tissue regeneration pathway counters Leukotriene D4-stimulated vascular responses.
    'FASEB', 2018
    Co-Authors: Chiang N, Dalli J, Ir Riley, Ar Rodriguez, Bw Spur, Cn Serhan
    Abstract:

    Resolution of acute inflammation is governed, in part, by lipid mediator class switching from proinflammatory eicosanoids to specialized proresolving mediators, including a recently identified new pathway of mediators, termed maresin conjugates in tissue regeneration (MCTR), which includes MCTR1, MCTR2, and MCTR3. Here, we addressed whether each MCTR can impact the known vascular actions of cysteinyl Leukotrienes. Leukotriene D4 (LTD4; 1.5 nmol/mouse) initiated vascular leakage in mouse cremaster vessels, which was reduced (>75%) by MCTR1 and MCTR2 (0.15 nmol each). With isolated Ciona intestinalis (sea squirt) primordial hearts, LTD4 (1-100 nM) induced negative inotropic action and lowered heartbeats 20-30%. Each MCTR (1-100 nM) prevented LTD4-reduced heart rates. With human cysteinyl Leukotriene receptor-1 (CysLT1) expressed in CHO cells, each MCTR (10-100 nM) significantly reduced LTD4-initiated signaling. To assess the contribution of CysLT1 in the proresolving actions of MCTR, we carried out human macrophage (MΦ) phagocytosis. Each MCTR (0.1-10 nM) stimulated human MΦ phagocytosis of live Escherichia coli, whereas LTD4 did not stimulate phagocytosis. MCTR-activated phagocytosis was significantly blocked by a pharmacologic receptor antagonist (MK571). With both CHO-CysLT1 and human MΦs, each MCTR competed for specific [3H]-LTD4 binding with apparent lower affinity than LTD4. Thus, each MCTR functionally interacts with human CysLT1 to pharmacologically counter-regulate vascular responses and stimulate physiologic phagocytosis with MΦs.-Chiang, N., Riley, I. R., Dalli, J., Rodriguez, A. R., Spur, B. W., Serhan, C. N. New maresin conjugates in tissue regeneration pathway counters Leukotriene D4-stimulated vascular responses.This work was supported, in part, by U.S. National Institutes of Health, National Institute of General Medical Sciences Grants P01-GM095467 and R01-GM38765 (to C.N.S.

D Berild - One of the best experts on this subject based on the ideXlab platform.

  • Possible existence of Leukotriene D4 receptors and mechanism of their signal transduction in human polymorphonuclear leukocytes.
    Scandinavian journal of clinical and laboratory investigation. Supplementum, 1991
    Co-Authors: P N Bouchelouche, D Berild
    Abstract:

    Previous work from this laboratory has demonstrated that stimulation of human polymorphonuclear leukocytes (PMN) with the peptidyl Leukotriene D4 (LTD4) results in the formation of second messenger signals, i.e. mobilization of intracellular free Ca2+ ([Ca2+]i) and hydrolysis of phosphoinositides (PIP2). Based on these earlier results we have employed radioligand binding techniques to study the presence of LTD4 receptors in intact human PMN leukocytes. The binding of [3H]-LTD4 to LTD4 receptors is rapid, reversible, specific and saturable. Scatchard analysis of the binding data indicates the presence of 116-275 identical receptors per neutrophil with an apparent dissociation constant (KD) of 1,1-2,3 nM. Only one class of binding sites was identified. The LTD4 receptors are located in the plasma membrane and are specific for LTD4 since binding is unaffected by other Leukotrienes. Furthermore, LTD4 induces a rapid and persistent translocation of Protein Kinase C (PKC) from the cytosol to the membrane. The LTD4 binding and PKC translocation could be blocked in a concentration dependent manner by the new and specific LTD4 receptor antagonist ICI 198,615. These observations strongly suggest that human PMN might possess specific LTD4 receptors which are coupled to the inositol trisphosphate pathway resulting in a rise in the cytoplasmic free Ca2+ and redistribution of protein kinase C. A mechanism of signal transduction for Leukotriene D4 is proposed.