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Roberto Levi - One of the best experts on this subject based on the ideXlab platform.
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The novel H2S donor 4‐carboxy‐phenyl isothiocyanate inhibits mast cell degranulation and renin release by decreasing intracellular calcium
British Journal of Pharmacology, 2016Co-Authors: Alice Marino, Valentina Citi, Alma Martelli, Vincenzo Calderone, Ming Fu, Rui Wang, Roberto LeviAbstract:Background and Purpose Hydrogen sulfide (H2S) modulates many pathophysiological processes, including inflammation and allergic reactions, in which mast cells act as major effector cells. IgE receptor (FceRI) cross-linking leads to an increase in intracellular calcium ([Ca+2]i), a critical step in mast cell degranulation. The aim of this study was to investigate the role of H2S in [Ca+2]i-dependent mast cell Activation. Experimental Approach We investigated the effects of H2S, either endogenously produced or released by the slow H2S donor 4-carboxy-phenyl isothiocyanate (PhNCS-COOH), on antigenic- and non-antigenic degranulation of native murine mast cells (BMMC), human (HMC-1) and rat (RBL-2H3) mast cell lines. We measured the release of specific mast cell degranulation markers (β-hexosaminidase and renin), as well as changes in [Ca+2]i and phosphorylation of proteins downstream of FceRI Activation. Key Results Endogenously produced H2S inhibited antigen-induced degranulation in RBL-2H3. Similarly, H2S released by PhNCS-COOH (10-300 μM) reduced, in a concentration-dependent manner, antigenic and non-antigenic degranulation and renin release in all mast cell types. Notably, PhNCS-COOH also prevented in a concentration-dependent mode the increase in [Ca+2]i elicited by Ca+2 ionophore, thapsigargin and FceRI Activation. Moreover, PhNCS-COOH attenuated the phosphorylation of Syk, cPLA-2 and PLCγ1 in antigen-stimulated RBL-2H3 cells. Conclusion and Implications Collectively, our results demonstrate that, by attenuating the phosphorylation of proteins downstream of FceRI cross-linking on mast cells, H2S diminishes [Ca+2]i availability and thus, mast cell degranulation and renin release. These findings suggest that PhNCS-COOH could be a strategic therapeutic tool in mast cell-mediated allergic conditions. This article is protected by copyright. All rights reserved.
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the novel h2s donor 4 carboxy phenyl isothiocyanate inhibits mast cell degranulation and renin release by decreasing intracellular calcium
British Journal of Pharmacology, 2016Co-Authors: Alice Marino, Valentina Citi, Alma Martelli, Vincenzo Calderone, Ming Fu, Rui Wang, Roberto LeviAbstract:Background and Purpose Hydrogen sulfide (H2S) modulates many pathophysiological processes, including inflammation and allergic reactions, in which mast cells act as major effector cells. IgE receptor (FceRI) cross-linking leads to an increase in intracellular calcium ([Ca+2]i), a critical step in mast cell degranulation. The aim of this study was to investigate the role of H2S in [Ca+2]i-dependent mast cell Activation. Experimental Approach We investigated the effects of H2S, either endogenously produced or released by the slow H2S donor 4-carboxy-phenyl isothiocyanate (PhNCS-COOH), on antigenic- and non-antigenic degranulation of native murine mast cells (BMMC), human (HMC-1) and rat (RBL-2H3) mast cell lines. We measured the release of specific mast cell degranulation markers (β-hexosaminidase and renin), as well as changes in [Ca+2]i and phosphorylation of proteins downstream of FceRI Activation. Key Results Endogenously produced H2S inhibited antigen-induced degranulation in RBL-2H3. Similarly, H2S released by PhNCS-COOH (10-300 μM) reduced, in a concentration-dependent manner, antigenic and non-antigenic degranulation and renin release in all mast cell types. Notably, PhNCS-COOH also prevented in a concentration-dependent mode the increase in [Ca+2]i elicited by Ca+2 ionophore, thapsigargin and FceRI Activation. Moreover, PhNCS-COOH attenuated the phosphorylation of Syk, cPLA-2 and PLCγ1 in antigen-stimulated RBL-2H3 cells. Conclusion and Implications Collectively, our results demonstrate that, by attenuating the phosphorylation of proteins downstream of FceRI cross-linking on mast cells, H2S diminishes [Ca+2]i availability and thus, mast cell degranulation and renin release. These findings suggest that PhNCS-COOH could be a strategic therapeutic tool in mast cell-mediated allergic conditions. This article is protected by copyright. All rights reserved.
Alice Marino - One of the best experts on this subject based on the ideXlab platform.
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The novel H2S donor 4‐carboxy‐phenyl isothiocyanate inhibits mast cell degranulation and renin release by decreasing intracellular calcium
British Journal of Pharmacology, 2016Co-Authors: Alice Marino, Valentina Citi, Alma Martelli, Vincenzo Calderone, Ming Fu, Rui Wang, Roberto LeviAbstract:Background and Purpose Hydrogen sulfide (H2S) modulates many pathophysiological processes, including inflammation and allergic reactions, in which mast cells act as major effector cells. IgE receptor (FceRI) cross-linking leads to an increase in intracellular calcium ([Ca+2]i), a critical step in mast cell degranulation. The aim of this study was to investigate the role of H2S in [Ca+2]i-dependent mast cell Activation. Experimental Approach We investigated the effects of H2S, either endogenously produced or released by the slow H2S donor 4-carboxy-phenyl isothiocyanate (PhNCS-COOH), on antigenic- and non-antigenic degranulation of native murine mast cells (BMMC), human (HMC-1) and rat (RBL-2H3) mast cell lines. We measured the release of specific mast cell degranulation markers (β-hexosaminidase and renin), as well as changes in [Ca+2]i and phosphorylation of proteins downstream of FceRI Activation. Key Results Endogenously produced H2S inhibited antigen-induced degranulation in RBL-2H3. Similarly, H2S released by PhNCS-COOH (10-300 μM) reduced, in a concentration-dependent manner, antigenic and non-antigenic degranulation and renin release in all mast cell types. Notably, PhNCS-COOH also prevented in a concentration-dependent mode the increase in [Ca+2]i elicited by Ca+2 ionophore, thapsigargin and FceRI Activation. Moreover, PhNCS-COOH attenuated the phosphorylation of Syk, cPLA-2 and PLCγ1 in antigen-stimulated RBL-2H3 cells. Conclusion and Implications Collectively, our results demonstrate that, by attenuating the phosphorylation of proteins downstream of FceRI cross-linking on mast cells, H2S diminishes [Ca+2]i availability and thus, mast cell degranulation and renin release. These findings suggest that PhNCS-COOH could be a strategic therapeutic tool in mast cell-mediated allergic conditions. This article is protected by copyright. All rights reserved.
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the novel h2s donor 4 carboxy phenyl isothiocyanate inhibits mast cell degranulation and renin release by decreasing intracellular calcium
British Journal of Pharmacology, 2016Co-Authors: Alice Marino, Valentina Citi, Alma Martelli, Vincenzo Calderone, Ming Fu, Rui Wang, Roberto LeviAbstract:Background and Purpose Hydrogen sulfide (H2S) modulates many pathophysiological processes, including inflammation and allergic reactions, in which mast cells act as major effector cells. IgE receptor (FceRI) cross-linking leads to an increase in intracellular calcium ([Ca+2]i), a critical step in mast cell degranulation. The aim of this study was to investigate the role of H2S in [Ca+2]i-dependent mast cell Activation. Experimental Approach We investigated the effects of H2S, either endogenously produced or released by the slow H2S donor 4-carboxy-phenyl isothiocyanate (PhNCS-COOH), on antigenic- and non-antigenic degranulation of native murine mast cells (BMMC), human (HMC-1) and rat (RBL-2H3) mast cell lines. We measured the release of specific mast cell degranulation markers (β-hexosaminidase and renin), as well as changes in [Ca+2]i and phosphorylation of proteins downstream of FceRI Activation. Key Results Endogenously produced H2S inhibited antigen-induced degranulation in RBL-2H3. Similarly, H2S released by PhNCS-COOH (10-300 μM) reduced, in a concentration-dependent manner, antigenic and non-antigenic degranulation and renin release in all mast cell types. Notably, PhNCS-COOH also prevented in a concentration-dependent mode the increase in [Ca+2]i elicited by Ca+2 ionophore, thapsigargin and FceRI Activation. Moreover, PhNCS-COOH attenuated the phosphorylation of Syk, cPLA-2 and PLCγ1 in antigen-stimulated RBL-2H3 cells. Conclusion and Implications Collectively, our results demonstrate that, by attenuating the phosphorylation of proteins downstream of FceRI cross-linking on mast cells, H2S diminishes [Ca+2]i availability and thus, mast cell degranulation and renin release. These findings suggest that PhNCS-COOH could be a strategic therapeutic tool in mast cell-mediated allergic conditions. This article is protected by copyright. All rights reserved.
Alma Martelli - One of the best experts on this subject based on the ideXlab platform.
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The novel H2S donor 4‐carboxy‐phenyl isothiocyanate inhibits mast cell degranulation and renin release by decreasing intracellular calcium
British Journal of Pharmacology, 2016Co-Authors: Alice Marino, Valentina Citi, Alma Martelli, Vincenzo Calderone, Ming Fu, Rui Wang, Roberto LeviAbstract:Background and Purpose Hydrogen sulfide (H2S) modulates many pathophysiological processes, including inflammation and allergic reactions, in which mast cells act as major effector cells. IgE receptor (FceRI) cross-linking leads to an increase in intracellular calcium ([Ca+2]i), a critical step in mast cell degranulation. The aim of this study was to investigate the role of H2S in [Ca+2]i-dependent mast cell Activation. Experimental Approach We investigated the effects of H2S, either endogenously produced or released by the slow H2S donor 4-carboxy-phenyl isothiocyanate (PhNCS-COOH), on antigenic- and non-antigenic degranulation of native murine mast cells (BMMC), human (HMC-1) and rat (RBL-2H3) mast cell lines. We measured the release of specific mast cell degranulation markers (β-hexosaminidase and renin), as well as changes in [Ca+2]i and phosphorylation of proteins downstream of FceRI Activation. Key Results Endogenously produced H2S inhibited antigen-induced degranulation in RBL-2H3. Similarly, H2S released by PhNCS-COOH (10-300 μM) reduced, in a concentration-dependent manner, antigenic and non-antigenic degranulation and renin release in all mast cell types. Notably, PhNCS-COOH also prevented in a concentration-dependent mode the increase in [Ca+2]i elicited by Ca+2 ionophore, thapsigargin and FceRI Activation. Moreover, PhNCS-COOH attenuated the phosphorylation of Syk, cPLA-2 and PLCγ1 in antigen-stimulated RBL-2H3 cells. Conclusion and Implications Collectively, our results demonstrate that, by attenuating the phosphorylation of proteins downstream of FceRI cross-linking on mast cells, H2S diminishes [Ca+2]i availability and thus, mast cell degranulation and renin release. These findings suggest that PhNCS-COOH could be a strategic therapeutic tool in mast cell-mediated allergic conditions. This article is protected by copyright. All rights reserved.
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the novel h2s donor 4 carboxy phenyl isothiocyanate inhibits mast cell degranulation and renin release by decreasing intracellular calcium
British Journal of Pharmacology, 2016Co-Authors: Alice Marino, Valentina Citi, Alma Martelli, Vincenzo Calderone, Ming Fu, Rui Wang, Roberto LeviAbstract:Background and Purpose Hydrogen sulfide (H2S) modulates many pathophysiological processes, including inflammation and allergic reactions, in which mast cells act as major effector cells. IgE receptor (FceRI) cross-linking leads to an increase in intracellular calcium ([Ca+2]i), a critical step in mast cell degranulation. The aim of this study was to investigate the role of H2S in [Ca+2]i-dependent mast cell Activation. Experimental Approach We investigated the effects of H2S, either endogenously produced or released by the slow H2S donor 4-carboxy-phenyl isothiocyanate (PhNCS-COOH), on antigenic- and non-antigenic degranulation of native murine mast cells (BMMC), human (HMC-1) and rat (RBL-2H3) mast cell lines. We measured the release of specific mast cell degranulation markers (β-hexosaminidase and renin), as well as changes in [Ca+2]i and phosphorylation of proteins downstream of FceRI Activation. Key Results Endogenously produced H2S inhibited antigen-induced degranulation in RBL-2H3. Similarly, H2S released by PhNCS-COOH (10-300 μM) reduced, in a concentration-dependent manner, antigenic and non-antigenic degranulation and renin release in all mast cell types. Notably, PhNCS-COOH also prevented in a concentration-dependent mode the increase in [Ca+2]i elicited by Ca+2 ionophore, thapsigargin and FceRI Activation. Moreover, PhNCS-COOH attenuated the phosphorylation of Syk, cPLA-2 and PLCγ1 in antigen-stimulated RBL-2H3 cells. Conclusion and Implications Collectively, our results demonstrate that, by attenuating the phosphorylation of proteins downstream of FceRI cross-linking on mast cells, H2S diminishes [Ca+2]i availability and thus, mast cell degranulation and renin release. These findings suggest that PhNCS-COOH could be a strategic therapeutic tool in mast cell-mediated allergic conditions. This article is protected by copyright. All rights reserved.
Valentina Citi - One of the best experts on this subject based on the ideXlab platform.
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The novel H2S donor 4‐carboxy‐phenyl isothiocyanate inhibits mast cell degranulation and renin release by decreasing intracellular calcium
British Journal of Pharmacology, 2016Co-Authors: Alice Marino, Valentina Citi, Alma Martelli, Vincenzo Calderone, Ming Fu, Rui Wang, Roberto LeviAbstract:Background and Purpose Hydrogen sulfide (H2S) modulates many pathophysiological processes, including inflammation and allergic reactions, in which mast cells act as major effector cells. IgE receptor (FceRI) cross-linking leads to an increase in intracellular calcium ([Ca+2]i), a critical step in mast cell degranulation. The aim of this study was to investigate the role of H2S in [Ca+2]i-dependent mast cell Activation. Experimental Approach We investigated the effects of H2S, either endogenously produced or released by the slow H2S donor 4-carboxy-phenyl isothiocyanate (PhNCS-COOH), on antigenic- and non-antigenic degranulation of native murine mast cells (BMMC), human (HMC-1) and rat (RBL-2H3) mast cell lines. We measured the release of specific mast cell degranulation markers (β-hexosaminidase and renin), as well as changes in [Ca+2]i and phosphorylation of proteins downstream of FceRI Activation. Key Results Endogenously produced H2S inhibited antigen-induced degranulation in RBL-2H3. Similarly, H2S released by PhNCS-COOH (10-300 μM) reduced, in a concentration-dependent manner, antigenic and non-antigenic degranulation and renin release in all mast cell types. Notably, PhNCS-COOH also prevented in a concentration-dependent mode the increase in [Ca+2]i elicited by Ca+2 ionophore, thapsigargin and FceRI Activation. Moreover, PhNCS-COOH attenuated the phosphorylation of Syk, cPLA-2 and PLCγ1 in antigen-stimulated RBL-2H3 cells. Conclusion and Implications Collectively, our results demonstrate that, by attenuating the phosphorylation of proteins downstream of FceRI cross-linking on mast cells, H2S diminishes [Ca+2]i availability and thus, mast cell degranulation and renin release. These findings suggest that PhNCS-COOH could be a strategic therapeutic tool in mast cell-mediated allergic conditions. This article is protected by copyright. All rights reserved.
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the novel h2s donor 4 carboxy phenyl isothiocyanate inhibits mast cell degranulation and renin release by decreasing intracellular calcium
British Journal of Pharmacology, 2016Co-Authors: Alice Marino, Valentina Citi, Alma Martelli, Vincenzo Calderone, Ming Fu, Rui Wang, Roberto LeviAbstract:Background and Purpose Hydrogen sulfide (H2S) modulates many pathophysiological processes, including inflammation and allergic reactions, in which mast cells act as major effector cells. IgE receptor (FceRI) cross-linking leads to an increase in intracellular calcium ([Ca+2]i), a critical step in mast cell degranulation. The aim of this study was to investigate the role of H2S in [Ca+2]i-dependent mast cell Activation. Experimental Approach We investigated the effects of H2S, either endogenously produced or released by the slow H2S donor 4-carboxy-phenyl isothiocyanate (PhNCS-COOH), on antigenic- and non-antigenic degranulation of native murine mast cells (BMMC), human (HMC-1) and rat (RBL-2H3) mast cell lines. We measured the release of specific mast cell degranulation markers (β-hexosaminidase and renin), as well as changes in [Ca+2]i and phosphorylation of proteins downstream of FceRI Activation. Key Results Endogenously produced H2S inhibited antigen-induced degranulation in RBL-2H3. Similarly, H2S released by PhNCS-COOH (10-300 μM) reduced, in a concentration-dependent manner, antigenic and non-antigenic degranulation and renin release in all mast cell types. Notably, PhNCS-COOH also prevented in a concentration-dependent mode the increase in [Ca+2]i elicited by Ca+2 ionophore, thapsigargin and FceRI Activation. Moreover, PhNCS-COOH attenuated the phosphorylation of Syk, cPLA-2 and PLCγ1 in antigen-stimulated RBL-2H3 cells. Conclusion and Implications Collectively, our results demonstrate that, by attenuating the phosphorylation of proteins downstream of FceRI cross-linking on mast cells, H2S diminishes [Ca+2]i availability and thus, mast cell degranulation and renin release. These findings suggest that PhNCS-COOH could be a strategic therapeutic tool in mast cell-mediated allergic conditions. This article is protected by copyright. All rights reserved.
Rui Wang - One of the best experts on this subject based on the ideXlab platform.
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The novel H2S donor 4‐carboxy‐phenyl isothiocyanate inhibits mast cell degranulation and renin release by decreasing intracellular calcium
British Journal of Pharmacology, 2016Co-Authors: Alice Marino, Valentina Citi, Alma Martelli, Vincenzo Calderone, Ming Fu, Rui Wang, Roberto LeviAbstract:Background and Purpose Hydrogen sulfide (H2S) modulates many pathophysiological processes, including inflammation and allergic reactions, in which mast cells act as major effector cells. IgE receptor (FceRI) cross-linking leads to an increase in intracellular calcium ([Ca+2]i), a critical step in mast cell degranulation. The aim of this study was to investigate the role of H2S in [Ca+2]i-dependent mast cell Activation. Experimental Approach We investigated the effects of H2S, either endogenously produced or released by the slow H2S donor 4-carboxy-phenyl isothiocyanate (PhNCS-COOH), on antigenic- and non-antigenic degranulation of native murine mast cells (BMMC), human (HMC-1) and rat (RBL-2H3) mast cell lines. We measured the release of specific mast cell degranulation markers (β-hexosaminidase and renin), as well as changes in [Ca+2]i and phosphorylation of proteins downstream of FceRI Activation. Key Results Endogenously produced H2S inhibited antigen-induced degranulation in RBL-2H3. Similarly, H2S released by PhNCS-COOH (10-300 μM) reduced, in a concentration-dependent manner, antigenic and non-antigenic degranulation and renin release in all mast cell types. Notably, PhNCS-COOH also prevented in a concentration-dependent mode the increase in [Ca+2]i elicited by Ca+2 ionophore, thapsigargin and FceRI Activation. Moreover, PhNCS-COOH attenuated the phosphorylation of Syk, cPLA-2 and PLCγ1 in antigen-stimulated RBL-2H3 cells. Conclusion and Implications Collectively, our results demonstrate that, by attenuating the phosphorylation of proteins downstream of FceRI cross-linking on mast cells, H2S diminishes [Ca+2]i availability and thus, mast cell degranulation and renin release. These findings suggest that PhNCS-COOH could be a strategic therapeutic tool in mast cell-mediated allergic conditions. This article is protected by copyright. All rights reserved.
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the novel h2s donor 4 carboxy phenyl isothiocyanate inhibits mast cell degranulation and renin release by decreasing intracellular calcium
British Journal of Pharmacology, 2016Co-Authors: Alice Marino, Valentina Citi, Alma Martelli, Vincenzo Calderone, Ming Fu, Rui Wang, Roberto LeviAbstract:Background and Purpose Hydrogen sulfide (H2S) modulates many pathophysiological processes, including inflammation and allergic reactions, in which mast cells act as major effector cells. IgE receptor (FceRI) cross-linking leads to an increase in intracellular calcium ([Ca+2]i), a critical step in mast cell degranulation. The aim of this study was to investigate the role of H2S in [Ca+2]i-dependent mast cell Activation. Experimental Approach We investigated the effects of H2S, either endogenously produced or released by the slow H2S donor 4-carboxy-phenyl isothiocyanate (PhNCS-COOH), on antigenic- and non-antigenic degranulation of native murine mast cells (BMMC), human (HMC-1) and rat (RBL-2H3) mast cell lines. We measured the release of specific mast cell degranulation markers (β-hexosaminidase and renin), as well as changes in [Ca+2]i and phosphorylation of proteins downstream of FceRI Activation. Key Results Endogenously produced H2S inhibited antigen-induced degranulation in RBL-2H3. Similarly, H2S released by PhNCS-COOH (10-300 μM) reduced, in a concentration-dependent manner, antigenic and non-antigenic degranulation and renin release in all mast cell types. Notably, PhNCS-COOH also prevented in a concentration-dependent mode the increase in [Ca+2]i elicited by Ca+2 ionophore, thapsigargin and FceRI Activation. Moreover, PhNCS-COOH attenuated the phosphorylation of Syk, cPLA-2 and PLCγ1 in antigen-stimulated RBL-2H3 cells. Conclusion and Implications Collectively, our results demonstrate that, by attenuating the phosphorylation of proteins downstream of FceRI cross-linking on mast cells, H2S diminishes [Ca+2]i availability and thus, mast cell degranulation and renin release. These findings suggest that PhNCS-COOH could be a strategic therapeutic tool in mast cell-mediated allergic conditions. This article is protected by copyright. All rights reserved.
