Details
- Autor(en) / Beteiligte
- Titel
- Hydrogen sulfide attenuated tumor necrosis factor-α-induced inflammatory signaling and dysfunction in vascular endothelial cells
- Ist Teil von
- PloS one, 2011-05, Vol.6 (5), p.e19766
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2011
- Link zum Volltext
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Hydrogen sulfide (H(2)S), the third physiologically relevant gaseous molecule, is recognized increasingly as an anti-inflammatory mediator in various inflammatory conditions. Herein, we explored the effects and mechanisms of sodium hydrosulfide (NaHS, a H(2)S donor) on tumor necrosis factor (TNF)-α-induced human umbilical vein endothelial cells (HUVEC) dysfunction. Application of NaHS concentration-dependently suppressed TNF-α-induced mRNA and proteins expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), mRNA expression of P-selectin and E-selectin as well as U937 monocytes adhesion to HUVEC. Western blot analysis revealed that the expression of the cytoprotective enzyme, heme oxygenase-1 (HO-1), was induced and coincident with the anti-inflammatory action of NaHS. Furthermore, TNF-α-induced NF-κB activation assessed by IκBα degradation and p65 phosphorylation and nuclear translocation and ROS production were diminished in cells subjected to treatment with NaHS. H(2)S can exert an anti-inflammatory effect in endothelial cells through a mechanism that involves the up-regulation of HO-1.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0019766Titel-ID: cdi_plos_journals_1295077849
- Format
- –
- Schlagworte
- Adhesion, Biology, Cell adhesion, Cell adhesion & migration, Cell Adhesion - drug effects, Cell adhesion molecules, Cell Nucleus - drug effects, Cell Nucleus - metabolism, Cytokines, E-selectin, Endothelial cells, Endothelial Cells - drug effects, Endothelial Cells - enzymology, Endothelial Cells - pathology, Endothelium, Enzyme Activation - drug effects, Gene expression, Heme, Heme oxygenase (decyclizing), Heme Oxygenase-1 - genetics, Heme Oxygenase-1 - metabolism, Humans, Hydrogen, Hydrogen ion concentration, Hydrogen sulfide, I-kappa B Proteins - metabolism, Inflammation, Inflammation - metabolism, Inflammation - pathology, Intercellular adhesion molecule 1, Intercellular Adhesion Molecule-1 - genetics, Intercellular Adhesion Molecule-1 - metabolism, Intracellular Space - drug effects, Intracellular Space - metabolism, Kinases, Medicine, Monocytes, Necrosis, NF-KappaB Inhibitor alpha, NF-κB protein, Nuclear transport, Oxidative stress, Oxygenase, P-selectin, p38 Mitogen-Activated Protein Kinases - metabolism, Pharmacology, Pharmacy, Phosphorylation, Phosphorylation - drug effects, Protein Processing, Post-Translational - drug effects, Protein Transport - drug effects, Proteins, Reactive Oxygen Species - metabolism, RNA, Messenger - genetics, RNA, Messenger - metabolism, Rodents, Signal transduction, Signal Transduction - drug effects, Signaling, Sodium, Studies, Sulfide, Sulfides - pharmacology, Transcription Factor RelA - metabolism, Translocation, Tumor Necrosis Factor-alpha - pharmacology, Tumor necrosis factor-TNF, Tumor necrosis factor-α, U937 Cells, Umbilical vein, Up-Regulation - drug effects, Vascular cell adhesion molecule 1, Vascular Cell Adhesion Molecule-1 - genetics, Vascular Cell Adhesion Molecule-1 - metabolism