Sphingosine 1-Phosphate (S1P) Induced Interleukin-8 (IL-8) Release Is Mediated by S1P Receptor 2 and Nuclear Factor κB in BEAS-2B Cells
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{"title"=>"Sphingosine 1-phosphate (S1P) induced interleukin-8 (IL-8) release is mediated by S1P receptor 2 and nuclear factor kB in BEAS-2B cells", "type"=>"journal", "authors"=>[{"first_name"=>"Michael J.", "last_name"=>"O'Sullivan", "scopus_author_id"=>"55792149200"}, {"first_name"=>"Nobuaki", "last_name"=>"Hirota", "scopus_author_id"=>"14045011200"}, {"first_name"=>"James G.", "last_name"=>"Martin", "scopus_author_id"=>"35493942900"}], "year"=>2014, "source"=>"PLoS ONE", "identifiers"=>{"pmid"=>"24743449", "doi"=>"10.1371/journal.pone.0095566", "pui"=>"372999731", "issn"=>"19326203", "sgr"=>"84899738610", "scopus"=>"2-s2.0-84899738610"}, "id"=>"4e3b167e-5eea-3985-b49c-74a6afb20ccd", "abstract"=>"The airway epithelium may release pro-inflammatory cytokines and chemokines in the asthmatic airway. Sphingosine 1-phosphate (S1P) is a bioactive lipid, increased in the airways of asthmatics, that may trigger the release of the potent neutrophil chemoattractant Interleukin-8 (IL-8) by epithelial cells. S1P is a ligand for 5 G protein-coupled receptors, S1PR1-5. We wished to explore the mechanisms of S1P induced IL-8 secretion with regard to the receptor(s) and downstream signaling events involved. Our results indicate that S1P induced IL-8 release is mediated by S1PR2 and the transcription factor NF-kB. Since the Epidermal Growth Factor Receptor (EGFR) and reactive oxygen species (ROS) have been implicated in IL-8 release in response to activation of other G protein-coupled receptors, we examined their importance in S1P induced IL-8 release and established that they are not involved. This study reveals S1PR2 and NF-kB as potential therapeutic targets in neutrophilic airway diseases such as severe asthma.", "link"=>"http://www.mendeley.com/research/sphingosine-1phosphate-s1p-induced-interleukin8-il8-release-mediated-s1p-receptor-2-nuclear-factor-k", "reader_count"=>6, "reader_count_by_academic_status"=>{"Researcher"=>1, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>1, "Student > Master"=>2, "Other"=>1}, "reader_count_by_user_role"=>{"Researcher"=>1, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>1, "Student > Master"=>2, "Other"=>1}, "reader_count_by_subject_area"=>{"Agricultural and Biological Sciences"=>4, "Medicine and Dentistry"=>1, "Pharmacology, Toxicology and Pharmaceutical Science"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>4}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}}, "reader_count_by_country"=>{"Iran"=>1}, "group_count"=>0}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/1468089"], "description"=>"<p>(A) BEAS-2B cells were incubated for 30 minutes with 10 µM DCFH-DA. Free probe was washed with Hank’s buffer and baseline fluorescence was measured at 530 nm. Cells were then stimulated with S1P or vehicle and fluorescence intensity was measured every 5 minutes for one hour (n = 3). Analysis using repeated measures ANOVA revealed no difference between the two curves. (B) BEAS-2B cells were pretreated for 30 minutes with the general antioxidant N-acetyl cysteine (NAC) and then stimulated with S1P for 4 hours (n = 5). Culture medium was assessed for IL-8 concentration by ELISA. (C) BEAS-2B cells were pretreated for 30 minutes with the NADPH oxidase inhibitor DPI and then stimulated with S1P for 4 hours (n = 5). Culture medium was assessed for IL-8 concentration by ELISA. (n = 5). Data are representative of means+SE. ANOVA with Tukey post hoc pairwise comparisons *P<0.05, **P<0.01.</p>", "links"=>[], "tags"=>["anatomy", "biological tissue", "epithelium", "Epithelial cells", "Endocrine system", "Biochemistry", "lipids", "Lipid mediators", "cell biology", "Cell processes", "Cell cycle and cell division", "cytokinesis", "Signal transduction", "cell signaling", "G-protein signaling", "Molecular cell biology", "developmental biology", "Molecular development", "cytokines", "immunology", "Immune system", "physiology", "Endocrine physiology", "Growth factors", "Epidermal growth factor", "Immune physiology", "Respiratory physiology", "Pulmonology", "asthma", "induced", "il-8", "reactive", "beas-2b"], "article_id"=>1002285, "categories"=>["Biological Sciences"], "users"=>["Michael J. O’Sullivan", "Nobuaki Hirota", "James G. Martin"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0095566.g006", "stats"=>{"downloads"=>0, "page_views"=>4, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_S1P_induced_IL_8_release_is_not_dependent_on_the_production_of_reactive_oxygen_species_in_BEAS_2B_cells_/1002285", "title"=>"S1P induced IL-8 release is not dependent on the production of reactive oxygen species in BEAS-2B cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-04-17 02:51:45"}
  • {"files"=>["https://ndownloader.figshare.com/files/1468088"], "description"=>"<p>(A) BEAS-2B cells were pretreated for 30 minutes with the specific EGFR inhibitor AG 1478 and then stimulated with S1P for 4 hours (n = 7). Culture medium was assessed for IL-8 concentration by ELISA. (B) BEAS-2B cells transfected with control or EGFR specific siRNA were stimulated with S1P for 4 hours (n = 3). Culture medium was assessed for concentrations of IL-8 by ELISA (left). Knock-down efficacy is shown by western blot for total EGFR (170 kDa) with GAPDH loading control (37 kDa) (right). Quantification of total EGFR bands is shown (n = 4) (bottom left). (C) BEAS-2B cells were pretreated for 30 minutes with MMP inhibitors GM6001 or TAPI-1 and then stimulated with S1P for 4 hours (n = 3). Culture medium was assessed for IL-8 concentration by ELISA. Data are representative of means+SE. ANOVA with Tukey post hoc pairwise comparisons. *P<0.05, **P<0.01, ***P<0.001.</p>", "links"=>[], "tags"=>["anatomy", "biological tissue", "epithelium", "Epithelial cells", "Endocrine system", "Biochemistry", "lipids", "Lipid mediators", "cell biology", "Cell processes", "Cell cycle and cell division", "cytokinesis", "Signal transduction", "cell signaling", "G-protein signaling", "Molecular cell biology", "developmental biology", "Molecular development", "cytokines", "immunology", "Immune system", "physiology", "Endocrine physiology", "Growth factors", "Epidermal growth factor", "Immune physiology", "Respiratory physiology", "Pulmonology", "asthma", "induced", "il-8", "egfr", "beas-2b"], "article_id"=>1002284, "categories"=>["Biological Sciences"], "users"=>["Michael J. O’Sullivan", "Nobuaki Hirota", "James G. Martin"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0095566.g005", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_S1P_induced_IL_8_release_is_not_dependent_on_the_EGFR_in_BEAS_2B_cells_/1002284", "title"=>"S1P induced IL-8 release is not dependent on the EGFR in BEAS-2B cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-04-17 02:51:45"}
  • {"files"=>["https://ndownloader.figshare.com/files/1468085"], "description"=>"<p>BEAS-2B cells were pretreated for 30 minutes with (A) W 123 (n = 5), (B) JTE 013 (n = 5) or (C) CAY 10444 (n = 8), specific inhibitors of S1PR1, S1PR2 and S1PR3 respectively and then stimulated with S1P or vehicle for 4 hours. Culture supernatant was analyzed for IL-8 concentration by ELISA. Human airway smooth muscle cells were loaded with 10 µM Fura 2-AM, then treated with CAY10444 or vehicle (n = 5) for 30 minutes and intracellular calcium was measured by ratiometric fluorescence microscopy (E). Cells were stimulated with S1P (n = 5) and increases in resting intracellular calcium were recorded (F). Data are representative of means+SE. ANOVA with Tukey post hoc pairwise comparisons. **P<0.01, ***P<0.001.</p>", "links"=>[], "tags"=>["anatomy", "biological tissue", "epithelium", "Epithelial cells", "Endocrine system", "Biochemistry", "lipids", "Lipid mediators", "cell biology", "Cell processes", "Cell cycle and cell division", "cytokinesis", "Signal transduction", "cell signaling", "G-protein signaling", "Molecular cell biology", "developmental biology", "Molecular development", "cytokines", "immunology", "Immune system", "physiology", "Endocrine physiology", "Growth factors", "Epidermal growth factor", "Immune physiology", "Respiratory physiology", "Pulmonology", "asthma", "induced", "il-8", "mediated", "s1pr2", "beas-2b"], "article_id"=>1002281, "categories"=>["Biological Sciences"], "users"=>["Michael J. O’Sullivan", "Nobuaki Hirota", "James G. Martin"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0095566.g002", "stats"=>{"downloads"=>0, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_S1P_induced_IL_8_release_is_mediated_by_S1PR2_in_BEAS_2B_cells_/1002281", "title"=>"S1P induced IL-8 release is mediated by S1PR2 in BEAS-2B cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-04-17 02:51:45"}
  • {"files"=>["https://ndownloader.figshare.com/files/1468084"], "description"=>"<p>BEAS-2B cells were stimulated with various concentrations of S1P for 4 hours. Culture supernatant was analyzed for concentration of IL-8 by ELISA (n = 5). Data are representative of means+SE. ANOVA with Tukey post hoc pairwise comparisons. *P<0.05.</p>", "links"=>[], "tags"=>["anatomy", "biological tissue", "epithelium", "Epithelial cells", "Endocrine system", "Biochemistry", "lipids", "Lipid mediators", "cell biology", "Cell processes", "Cell cycle and cell division", "cytokinesis", "Signal transduction", "cell signaling", "G-protein signaling", "Molecular cell biology", "developmental biology", "Molecular development", "cytokines", "immunology", "Immune system", "physiology", "Endocrine physiology", "Growth factors", "Epidermal growth factor", "Immune physiology", "Respiratory physiology", "Pulmonology", "asthma", "il-8", "beas-2b"], "article_id"=>1002280, "categories"=>["Biological Sciences"], "users"=>["Michael J. O’Sullivan", "Nobuaki Hirota", "James G. Martin"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0095566.g001", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_S1P_induces_IL_8_release_in_BEAS_2B_cells_/1002280", "title"=>"S1P induces IL-8 release in BEAS-2B cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-04-17 02:51:45"}
  • {"files"=>["https://ndownloader.figshare.com/files/1468087"], "description"=>"<p>Nf-κB luciferase reporter BEAS-2B cells were pretreated with S1PR2 inhibitor JTE 013 for 30 minutes before stimulation with S1P for 4 hours (n = 3). Cell lysates were analyzed for luciferase activity by Tecan iControl plate reader. Data are representative of means+SE. ANOVA with Tukey post hoc pairwise comparisons. ***P<0.001.</p>", "links"=>[], "tags"=>["anatomy", "biological tissue", "epithelium", "Epithelial cells", "Endocrine system", "Biochemistry", "lipids", "Lipid mediators", "cell biology", "Cell processes", "Cell cycle and cell division", "cytokinesis", "Signal transduction", "cell signaling", "G-protein signaling", "Molecular cell biology", "developmental biology", "Molecular development", "cytokines", "immunology", "Immune system", "physiology", "Endocrine physiology", "Growth factors", "Epidermal growth factor", "Immune physiology", "Respiratory physiology", "Pulmonology", "asthma", "induced", "mediated", "s1pr2", "beas-2b"], "article_id"=>1002283, "categories"=>["Biological Sciences"], "users"=>["Michael J. O’Sullivan", "Nobuaki Hirota", "James G. Martin"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0095566.g004", "stats"=>{"downloads"=>0, "page_views"=>7, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_S1P_induced_Nf_954_B_activity_is_mediated_by_S1PR2_in_BEAS_2B_cells_/1002283", "title"=>"S1P induced Nf-κB activity is mediated by S1PR2 in BEAS-2B cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-04-17 02:51:45"}
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Relative Metric

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