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Article: Synergistic effect of SCF and TNF-α on the up-regulation of cell-surface expression of ICAM-1 on human leukemic mast cell line (HMC)-1 cells

TitleSynergistic effect of SCF and TNF-α on the up-regulation of cell-surface expression of ICAM-1 on human leukemic mast cell line (HMC)-1 cells
Authors
KeywordsMAPK
NF-κB
Adhesion molecule
Issue Date2005
Citation
Journal of Leukocyte Biology, 2005, v. 78, n. 1, p. 239-247 How to Cite?
AbstractIntercellular adhesion molecule-1 (ICAM-1) has been shown to play crucial roles in mast cell interaction with other inflammatory cells and recruitment into the inflamed tissue. In the present study, human mast cell line-1 (HMC-1) was stimulated with different cytokines including stem cell factor (SCF), tumor necrosis factor α (TNF-α), interleukin (IL)-13, IL-18, and IL-25. Cell-surface expression of ICAM-1 was assessed by flow cytometry. To elucidate the intracellular signal transduction regulating the ICAM-1 expression, phosphorylated extracellular signal-regulated kinase (ERK), phosphorylated p38 mitogen-activated protein kinase (MAPK), and nuclear factor (NF)-κB translocation were assessed by enzyme-linked immunosorbent assay. Results showed that SCF, TNF-κB, and IL-13 but not IL-18 and IL-25 could up-regulate the surface expression of ICAM-1 on HMC-1 cells. A synergistic effect of SCF and TNF-α on ICAM-1 expression was demonstrated. This synergistic effect was shown to be dose-dependently enhanced by SCF but not TNF-α. Results indicated that SCF activated ERK, and TNF-α activated the p38 MAPK and NF-κB pathway. Selective inhibitor of ERK, PD098059, and c-kit inhibitors, STI571 and PP1, suppressed the combined SCF and TNF-α-induced ICAM-1 expression. BAY117082 but not SB203580, which are the inhibitors of NF-κB and p38 MAPK, respectively, suppressed the TNF-α-induced ICAM-1 expression. Therefore, SCF and TNF-α acted through ERK and the NF-κB pathway to regulate the ICAM-1 expression and elicited the synergistic effect. In conclusion, our results provide insight for cross-talk between different signaling pathways that can help in understanding the fine control of adhesion molecule expression under the concerted effects of cytokines. © Society for Leukocyte Biology.
Persistent Identifierhttp://hdl.handle.net/10722/205696
ISSN
2015 Impact Factor: 4.165
2015 SCImago Journal Rankings: 2.463
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTsang, Chiman-
dc.contributor.authorWong, Chunkwok-
dc.contributor.authorIp, Waiki-
dc.contributor.authorLam, Ching-
dc.date.accessioned2014-10-06T08:02:13Z-
dc.date.available2014-10-06T08:02:13Z-
dc.date.issued2005-
dc.identifier.citationJournal of Leukocyte Biology, 2005, v. 78, n. 1, p. 239-247-
dc.identifier.issn0741-5400-
dc.identifier.urihttp://hdl.handle.net/10722/205696-
dc.description.abstractIntercellular adhesion molecule-1 (ICAM-1) has been shown to play crucial roles in mast cell interaction with other inflammatory cells and recruitment into the inflamed tissue. In the present study, human mast cell line-1 (HMC-1) was stimulated with different cytokines including stem cell factor (SCF), tumor necrosis factor α (TNF-α), interleukin (IL)-13, IL-18, and IL-25. Cell-surface expression of ICAM-1 was assessed by flow cytometry. To elucidate the intracellular signal transduction regulating the ICAM-1 expression, phosphorylated extracellular signal-regulated kinase (ERK), phosphorylated p38 mitogen-activated protein kinase (MAPK), and nuclear factor (NF)-κB translocation were assessed by enzyme-linked immunosorbent assay. Results showed that SCF, TNF-κB, and IL-13 but not IL-18 and IL-25 could up-regulate the surface expression of ICAM-1 on HMC-1 cells. A synergistic effect of SCF and TNF-α on ICAM-1 expression was demonstrated. This synergistic effect was shown to be dose-dependently enhanced by SCF but not TNF-α. Results indicated that SCF activated ERK, and TNF-α activated the p38 MAPK and NF-κB pathway. Selective inhibitor of ERK, PD098059, and c-kit inhibitors, STI571 and PP1, suppressed the combined SCF and TNF-α-induced ICAM-1 expression. BAY117082 but not SB203580, which are the inhibitors of NF-κB and p38 MAPK, respectively, suppressed the TNF-α-induced ICAM-1 expression. Therefore, SCF and TNF-α acted through ERK and the NF-κB pathway to regulate the ICAM-1 expression and elicited the synergistic effect. In conclusion, our results provide insight for cross-talk between different signaling pathways that can help in understanding the fine control of adhesion molecule expression under the concerted effects of cytokines. © Society for Leukocyte Biology.-
dc.languageeng-
dc.relation.ispartofJournal of Leukocyte Biology-
dc.subjectMAPK-
dc.subjectNF-κB-
dc.subjectAdhesion molecule-
dc.titleSynergistic effect of SCF and TNF-α on the up-regulation of cell-surface expression of ICAM-1 on human leukemic mast cell line (HMC)-1 cells-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1189/jlb.0704400-
dc.identifier.pmid15800027-
dc.identifier.scopuseid_2-s2.0-22144486538-
dc.identifier.volume78-
dc.identifier.issue1-
dc.identifier.spage239-
dc.identifier.epage247-
dc.identifier.isiWOS:000230291300028-

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