The Experts below are selected from a list of 42 Experts worldwide ranked by ideXlab platform

Mauro S G Pavao - One of the best experts on this subject based on the ideXlab platform.

  • selectin blocking activity of a fucosylated chondroitin sulfate glycosaminoglycan from sea cucumber effect on tumor metastasis and neutrophil recruitment
    Journal of Biological Chemistry, 2007
    Co-Authors: Lubor Borsig, Lianchun Wang, Moises C M Cavalcante, Larissa Cardiloreis, Paola L Ferreira, Paulo A S Mourao, Jeffrey D Esko, Mauro S G Pavao
    Abstract:

    Heparin is an excellent inhibitor of P- and L-selectin binding to the carbohydrate determinant, sialyl Lewis(x). As a consequence of its anti-selectin activity, heparin attenuates metastasis and Inflammation. Here we show that fucosylated chondroitin sulfate (FucCS), a polysaccharide isolated from sea cucumber composed of a chondroitin sulfate backbone substituted at the 3-position of the beta-D-glucuronic acid residues with 2,4-disulfated alpha-L-fucopyranosyl branches, is a potent inhibitor of P- and L-selectin binding to immobilized sialyl Lewis(x) and LS180 carcinoma cell attachment to immobilized P- and L-selectins. Inhibition occurs in a concentration-dependent manner. Furthermore, FucCS was 4-8-fold more potent than heparin in the inhibition of the P- and L-selectin-sialyl Lewis(x) interactions. No inhibition of E-selectin was observed. FucCS also inhibited Lung colonization by adenocarcinoma MC-38 cells in an experimental metastasis model in mice, as well as neutrophil recruitment in two models of Inflammation (thioglycollate-induced peritonitis and Lipopolysaccharide-Induced Lung Inflammation). Inhibition occurred at a dose that produces no significant change in plasma activated partial thromboplastin time. Removal of the sulfated fucose branches on the FucCS abolished the inhibitory effect in vitro and in vivo. Overall, the results suggest that invertebrate FucCS may be a potential alternative to heparin for blocking metastasis and inflammatory reactions without the undesirable side effects of anticoagulant heparin.

  • selectin blocking activity of a fucosylated chondroitin sulfate glycosaminoglycan from sea cucumber effect on tumor metastasis and neutrophil recruitment
    Journal of Biological Chemistry, 2007
    Co-Authors: Lubor Borsig, Lianchun Wang, Moises C M Cavalcante, Larissa Cardiloreis, Paola L Ferreira, Paulo A S Mourao, Jeffrey D Esko, Mauro S G Pavao
    Abstract:

    Abstract Heparin is an excellent inhibitor of P- and L-selectin binding to the carbohydrate determinant, sialyl Lewisx. As a consequence of its anti-selectin activity, heparin attenuates metastasis and Inflammation. Here we show that fucosylated chondroitin sulfate (FucCS), a polysaccharide isolated from sea cucumber composed of a chondroitin sulfate backbone substituted at the 3-position of the β-d-glucuronic acid residues with 2,4-disulfated α-l-fucopyranosyl branches, is a potent inhibitor of P- and L-selectin binding to immobilized sialyl Lewisx and LS180 carcinoma cell attachment to immobilized P- and L-selectins. Inhibition occurs in a concentration-dependent manner. Furthermore, FucCS was 4–8-fold more potent than heparin in the inhibition of the P- and L-selectin-sialyl Lewisx interactions. No inhibition of E-selectin was observed. FucCS also inhibited Lung colonization by adenocarcinoma MC-38 cells in an experimental metastasis model in mice, as well as neutrophil recruitment in two models of Inflammation (thioglycollate-induced peritonitis and Lipopolysaccharide-Induced Lung Inflammation). Inhibition occurred at a dose that produces no significant change in plasma activated partial thromboplastin time. Removal of the sulfated fucose branches on the FucCS abolished the inhibitory effect in vitro and in vivo. Overall, the results suggest that invertebrate FucCS may be a potential alternative to heparin for blocking metastasis and inflammatory reactions without the undesirable side effects of anticoagulant heparin.

Sveneric Jordt - One of the best experts on this subject based on the ideXlab platform.

  • activation of a nerve injury transcriptional signature in airway innervating sensory neurons after lipopolysaccharide induced Lung Inflammation
    American Journal of Physiology-lung Cellular and Molecular Physiology, 2020
    Co-Authors: Melanie Maya Kaelberer, Ana Isabel Caceres, Sveneric Jordt
    Abstract:

    The Lungs and the immune and nervous systems functionally interact to respond to respiratory environmental exposures and infections. The Lungs are innervated by vagal sensory neurons of the jugular and nodose ganglia, fused together in smaller mammals as the jugular-nodose complex (JNC). Whereas the JNC shares properties with the other sensory ganglia, the trigeminal (TG) and dorsal root ganglia (DRG), these sensory structures express differential sets of genes that reflect their unique functionalities. Here, we used RNA sequencing (RNA-seq) in mice to identify the differential transcriptomes of the three sensory ganglia types. Using a fluorescent retrograde tracer and fluorescence-activated cell sorting, we isolated a defined population of airway-innervating JNC neurons and determined their differential transcriptional map after pulmonary exposure to lipopolysaccharide (LPS), a major mediator of acute Lung injury (ALI) and acute respiratory distress syndrome (ARDS) after infection with gram-negative bacteria or inhalation of organic dust. JNC neurons activated an injury response program, leading to increased expression of gene products such as the G protein-coupled receptor Cckbr, inducing functional changes in neuronal sensitivity to peptides, and Gpr151, also rapidly induced upon neuropathic nerve injury in pain models. Unique JNC-specific transcripts, present at only minimal levels in TG, DRG, and other organs, were identified. These included TMC3, encoding for a putative mechanosensor, and urotensin 2B, a hypertensive peptide. These findings highlight the unique properties of the JNC and reveal that ALI/ARDS rapidly induces a nerve injury-related state, changing vagal excitability.

  • activation of a nerve injury transcriptional signature in airway innervating sensory neurons after lipopolysaccharide induced Lung Inflammation
    bioRxiv, 2019
    Co-Authors: Melanie Maya Kaelberer, Ana Isabel Caceres, Sveneric Jordt
    Abstract:

    The Lungs, the immune and nervous systems functionally interact to respond to respiratory environmental exposures and infections. The Lungs are innervated by vagal sensory neurons of the jugular and nodose ganglia, fused together in smaller mammals as the jugular-nodose complex (JNC). While the JNC is similar to the other sensory ganglia, the trigeminal (TG) and dorsal root ganglia (DRG), these sensory structures express differential sets of genes that reflect their unique functionalities. Here, we used RNAseq in mice to identify the differential transcriptomes of the three sensory ganglia types. Using a fluorescent retrograde tracer and fluorescence-activated cell sorting we isolated a defined population of airway-innervating JNC neurons and determined their differential transcriptional map after pulmonary exposure to lipopolysaccharide (LPS), a major mediator of acute Lung injury (ALI) and acute respiratory distress syndrome (ARDS) after infection with Gram-negative bacteria or inhalation of organic dust. JNC neurons activated an injury response program leading to increased expression of gene products such as the G-protein coupled receptors, Cckbr, inducing functional changes in neuronal sensitivity to peptides, and Gpr151, also rapidly induced upon neuropathic nerve injury in pain models. Unique JNC-specific transcripts, present at only minimal levels in TG, DRG and other organs, were identified. These included TMC3, encoding for a putative mechano-sensor, and Urotensin 2B, a hypertensive peptide. These findings highlight the unique properties of the JNC and reveal that ALI/ARDS rapidly induce a nerve-injury related state changing vagal excitability.

Lubor Borsig - One of the best experts on this subject based on the ideXlab platform.

  • selectin blocking activity of a fucosylated chondroitin sulfate glycosaminoglycan from sea cucumber effect on tumor metastasis and neutrophil recruitment
    Journal of Biological Chemistry, 2007
    Co-Authors: Lubor Borsig, Lianchun Wang, Moises C M Cavalcante, Larissa Cardiloreis, Paola L Ferreira, Paulo A S Mourao, Jeffrey D Esko, Mauro S G Pavao
    Abstract:

    Heparin is an excellent inhibitor of P- and L-selectin binding to the carbohydrate determinant, sialyl Lewis(x). As a consequence of its anti-selectin activity, heparin attenuates metastasis and Inflammation. Here we show that fucosylated chondroitin sulfate (FucCS), a polysaccharide isolated from sea cucumber composed of a chondroitin sulfate backbone substituted at the 3-position of the beta-D-glucuronic acid residues with 2,4-disulfated alpha-L-fucopyranosyl branches, is a potent inhibitor of P- and L-selectin binding to immobilized sialyl Lewis(x) and LS180 carcinoma cell attachment to immobilized P- and L-selectins. Inhibition occurs in a concentration-dependent manner. Furthermore, FucCS was 4-8-fold more potent than heparin in the inhibition of the P- and L-selectin-sialyl Lewis(x) interactions. No inhibition of E-selectin was observed. FucCS also inhibited Lung colonization by adenocarcinoma MC-38 cells in an experimental metastasis model in mice, as well as neutrophil recruitment in two models of Inflammation (thioglycollate-induced peritonitis and Lipopolysaccharide-Induced Lung Inflammation). Inhibition occurred at a dose that produces no significant change in plasma activated partial thromboplastin time. Removal of the sulfated fucose branches on the FucCS abolished the inhibitory effect in vitro and in vivo. Overall, the results suggest that invertebrate FucCS may be a potential alternative to heparin for blocking metastasis and inflammatory reactions without the undesirable side effects of anticoagulant heparin.

  • selectin blocking activity of a fucosylated chondroitin sulfate glycosaminoglycan from sea cucumber effect on tumor metastasis and neutrophil recruitment
    Journal of Biological Chemistry, 2007
    Co-Authors: Lubor Borsig, Lianchun Wang, Moises C M Cavalcante, Larissa Cardiloreis, Paola L Ferreira, Paulo A S Mourao, Jeffrey D Esko, Mauro S G Pavao
    Abstract:

    Abstract Heparin is an excellent inhibitor of P- and L-selectin binding to the carbohydrate determinant, sialyl Lewisx. As a consequence of its anti-selectin activity, heparin attenuates metastasis and Inflammation. Here we show that fucosylated chondroitin sulfate (FucCS), a polysaccharide isolated from sea cucumber composed of a chondroitin sulfate backbone substituted at the 3-position of the β-d-glucuronic acid residues with 2,4-disulfated α-l-fucopyranosyl branches, is a potent inhibitor of P- and L-selectin binding to immobilized sialyl Lewisx and LS180 carcinoma cell attachment to immobilized P- and L-selectins. Inhibition occurs in a concentration-dependent manner. Furthermore, FucCS was 4–8-fold more potent than heparin in the inhibition of the P- and L-selectin-sialyl Lewisx interactions. No inhibition of E-selectin was observed. FucCS also inhibited Lung colonization by adenocarcinoma MC-38 cells in an experimental metastasis model in mice, as well as neutrophil recruitment in two models of Inflammation (thioglycollate-induced peritonitis and Lipopolysaccharide-Induced Lung Inflammation). Inhibition occurred at a dose that produces no significant change in plasma activated partial thromboplastin time. Removal of the sulfated fucose branches on the FucCS abolished the inhibitory effect in vitro and in vivo. Overall, the results suggest that invertebrate FucCS may be a potential alternative to heparin for blocking metastasis and inflammatory reactions without the undesirable side effects of anticoagulant heparin.

Melanie Maya Kaelberer - One of the best experts on this subject based on the ideXlab platform.

  • activation of a nerve injury transcriptional signature in airway innervating sensory neurons after lipopolysaccharide induced Lung Inflammation
    American Journal of Physiology-lung Cellular and Molecular Physiology, 2020
    Co-Authors: Melanie Maya Kaelberer, Ana Isabel Caceres, Sveneric Jordt
    Abstract:

    The Lungs and the immune and nervous systems functionally interact to respond to respiratory environmental exposures and infections. The Lungs are innervated by vagal sensory neurons of the jugular and nodose ganglia, fused together in smaller mammals as the jugular-nodose complex (JNC). Whereas the JNC shares properties with the other sensory ganglia, the trigeminal (TG) and dorsal root ganglia (DRG), these sensory structures express differential sets of genes that reflect their unique functionalities. Here, we used RNA sequencing (RNA-seq) in mice to identify the differential transcriptomes of the three sensory ganglia types. Using a fluorescent retrograde tracer and fluorescence-activated cell sorting, we isolated a defined population of airway-innervating JNC neurons and determined their differential transcriptional map after pulmonary exposure to lipopolysaccharide (LPS), a major mediator of acute Lung injury (ALI) and acute respiratory distress syndrome (ARDS) after infection with gram-negative bacteria or inhalation of organic dust. JNC neurons activated an injury response program, leading to increased expression of gene products such as the G protein-coupled receptor Cckbr, inducing functional changes in neuronal sensitivity to peptides, and Gpr151, also rapidly induced upon neuropathic nerve injury in pain models. Unique JNC-specific transcripts, present at only minimal levels in TG, DRG, and other organs, were identified. These included TMC3, encoding for a putative mechanosensor, and urotensin 2B, a hypertensive peptide. These findings highlight the unique properties of the JNC and reveal that ALI/ARDS rapidly induces a nerve injury-related state, changing vagal excitability.

  • activation of a nerve injury transcriptional signature in airway innervating sensory neurons after lipopolysaccharide induced Lung Inflammation
    bioRxiv, 2019
    Co-Authors: Melanie Maya Kaelberer, Ana Isabel Caceres, Sveneric Jordt
    Abstract:

    The Lungs, the immune and nervous systems functionally interact to respond to respiratory environmental exposures and infections. The Lungs are innervated by vagal sensory neurons of the jugular and nodose ganglia, fused together in smaller mammals as the jugular-nodose complex (JNC). While the JNC is similar to the other sensory ganglia, the trigeminal (TG) and dorsal root ganglia (DRG), these sensory structures express differential sets of genes that reflect their unique functionalities. Here, we used RNAseq in mice to identify the differential transcriptomes of the three sensory ganglia types. Using a fluorescent retrograde tracer and fluorescence-activated cell sorting we isolated a defined population of airway-innervating JNC neurons and determined their differential transcriptional map after pulmonary exposure to lipopolysaccharide (LPS), a major mediator of acute Lung injury (ALI) and acute respiratory distress syndrome (ARDS) after infection with Gram-negative bacteria or inhalation of organic dust. JNC neurons activated an injury response program leading to increased expression of gene products such as the G-protein coupled receptors, Cckbr, inducing functional changes in neuronal sensitivity to peptides, and Gpr151, also rapidly induced upon neuropathic nerve injury in pain models. Unique JNC-specific transcripts, present at only minimal levels in TG, DRG and other organs, were identified. These included TMC3, encoding for a putative mechano-sensor, and Urotensin 2B, a hypertensive peptide. These findings highlight the unique properties of the JNC and reveal that ALI/ARDS rapidly induce a nerve-injury related state changing vagal excitability.

Lianchun Wang - One of the best experts on this subject based on the ideXlab platform.

  • selectin blocking activity of a fucosylated chondroitin sulfate glycosaminoglycan from sea cucumber effect on tumor metastasis and neutrophil recruitment
    Journal of Biological Chemistry, 2007
    Co-Authors: Lubor Borsig, Lianchun Wang, Moises C M Cavalcante, Larissa Cardiloreis, Paola L Ferreira, Paulo A S Mourao, Jeffrey D Esko, Mauro S G Pavao
    Abstract:

    Heparin is an excellent inhibitor of P- and L-selectin binding to the carbohydrate determinant, sialyl Lewis(x). As a consequence of its anti-selectin activity, heparin attenuates metastasis and Inflammation. Here we show that fucosylated chondroitin sulfate (FucCS), a polysaccharide isolated from sea cucumber composed of a chondroitin sulfate backbone substituted at the 3-position of the beta-D-glucuronic acid residues with 2,4-disulfated alpha-L-fucopyranosyl branches, is a potent inhibitor of P- and L-selectin binding to immobilized sialyl Lewis(x) and LS180 carcinoma cell attachment to immobilized P- and L-selectins. Inhibition occurs in a concentration-dependent manner. Furthermore, FucCS was 4-8-fold more potent than heparin in the inhibition of the P- and L-selectin-sialyl Lewis(x) interactions. No inhibition of E-selectin was observed. FucCS also inhibited Lung colonization by adenocarcinoma MC-38 cells in an experimental metastasis model in mice, as well as neutrophil recruitment in two models of Inflammation (thioglycollate-induced peritonitis and Lipopolysaccharide-Induced Lung Inflammation). Inhibition occurred at a dose that produces no significant change in plasma activated partial thromboplastin time. Removal of the sulfated fucose branches on the FucCS abolished the inhibitory effect in vitro and in vivo. Overall, the results suggest that invertebrate FucCS may be a potential alternative to heparin for blocking metastasis and inflammatory reactions without the undesirable side effects of anticoagulant heparin.

  • selectin blocking activity of a fucosylated chondroitin sulfate glycosaminoglycan from sea cucumber effect on tumor metastasis and neutrophil recruitment
    Journal of Biological Chemistry, 2007
    Co-Authors: Lubor Borsig, Lianchun Wang, Moises C M Cavalcante, Larissa Cardiloreis, Paola L Ferreira, Paulo A S Mourao, Jeffrey D Esko, Mauro S G Pavao
    Abstract:

    Abstract Heparin is an excellent inhibitor of P- and L-selectin binding to the carbohydrate determinant, sialyl Lewisx. As a consequence of its anti-selectin activity, heparin attenuates metastasis and Inflammation. Here we show that fucosylated chondroitin sulfate (FucCS), a polysaccharide isolated from sea cucumber composed of a chondroitin sulfate backbone substituted at the 3-position of the β-d-glucuronic acid residues with 2,4-disulfated α-l-fucopyranosyl branches, is a potent inhibitor of P- and L-selectin binding to immobilized sialyl Lewisx and LS180 carcinoma cell attachment to immobilized P- and L-selectins. Inhibition occurs in a concentration-dependent manner. Furthermore, FucCS was 4–8-fold more potent than heparin in the inhibition of the P- and L-selectin-sialyl Lewisx interactions. No inhibition of E-selectin was observed. FucCS also inhibited Lung colonization by adenocarcinoma MC-38 cells in an experimental metastasis model in mice, as well as neutrophil recruitment in two models of Inflammation (thioglycollate-induced peritonitis and Lipopolysaccharide-Induced Lung Inflammation). Inhibition occurred at a dose that produces no significant change in plasma activated partial thromboplastin time. Removal of the sulfated fucose branches on the FucCS abolished the inhibitory effect in vitro and in vivo. Overall, the results suggest that invertebrate FucCS may be a potential alternative to heparin for blocking metastasis and inflammatory reactions without the undesirable side effects of anticoagulant heparin.