File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Molecular mechanisms for the release of chemokines from human leukemic mast cell line (HMC)-1 cells activated by SCF and TNF-α: Roles of ERK, p38 MAPK, and NF-κB

TitleMolecular mechanisms for the release of chemokines from human leukemic mast cell line (HMC)-1 cells activated by SCF and TNF-α: Roles of ERK, p38 MAPK, and NF-κB
Authors
KeywordsBasic mechanisms
Chemokines
Mast cells
Issue Date2006
Citation
Allergy: European Journal of Allergy and Clinical Immunology, 2006, v. 61, n. 3, p. 289-297 How to Cite?
AbstractBackground: Mast cells play pivotal roles in IgE-mediated airway inflammation and other mast cell-mediated inflammation by activation and chemoattraction of inflammatory cells. Objective: We investigated the intracellular signaling mechanisms regulating chemokine release from human mast cell line-1 (HMC-1) cells activated by stem cell factor (SCF) or tumor necrosis factor (TNF)-α. Methods: Chemokine gene expressions were assessed by reverse transcription-polymerase chain reaction, while the releases of chemokines were determined by flow cytometry or enzyme-linked immunosorbent assay (ELISA). To elucidate the intracellular signal transduction regulating the chemokine expression, phosphorylated-extracellular signal-regulated kinase (ERK), phosphorylated-p38 mitogen-activated protein kinase (MAPK) and nuclear translocated nuclear factor (NF)-κB-DNA binding were quantitatively assessed by ELISA. Results: Either SCF or TNF-α could induce release from HMC-1 cells of interleukin (IL)-8, monocyte chemoattractant protein (MCP)-1, regulated upon activation normal T-cell expressed and secreted (RANTES), and I-309, while SCF and TNF-α induced release of macrophage inflammatory protein (MIP)-1β and interferon-γ-inducible protein-10 (IP-10), respectively. Using various selective inhibitors for signaling molecules, we found that the inductions of IL-8, MCP-1, and I-309 were mediated by either SCF-activated ERK or TNF-α-activated p38 MAPK, while the induction of IP-10 by TNF-α was mediated by both activated p38 MAPK and NF-κB. The induction of RANTES by SCF or TNF-α was mediated by ERK and NF-κB, respectively, and SCF induced MIP-1β release was mediated by ERK. Conclusion: The above results therefore elucidated the different intracellular signaling pathways regulating the release of different chemokines from SCF and TNF-α-activated mast cells, thereby shedding light for the immunopathological mechanisms of mast cell-mediated diseases. Copyright © Blackwell Munksgaard 2006.
Persistent Identifierhttp://hdl.handle.net/10722/205699
ISSN
2015 Impact Factor: 6.335
2015 SCImago Journal Rankings: 3.048
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWong, Chunkwok-
dc.contributor.authorTsang, Chiman-
dc.contributor.authorIp, Waiki-
dc.contributor.authorLam, Ching-
dc.date.accessioned2014-10-06T08:02:13Z-
dc.date.available2014-10-06T08:02:13Z-
dc.date.issued2006-
dc.identifier.citationAllergy: European Journal of Allergy and Clinical Immunology, 2006, v. 61, n. 3, p. 289-297-
dc.identifier.issn0105-4538-
dc.identifier.urihttp://hdl.handle.net/10722/205699-
dc.description.abstractBackground: Mast cells play pivotal roles in IgE-mediated airway inflammation and other mast cell-mediated inflammation by activation and chemoattraction of inflammatory cells. Objective: We investigated the intracellular signaling mechanisms regulating chemokine release from human mast cell line-1 (HMC-1) cells activated by stem cell factor (SCF) or tumor necrosis factor (TNF)-α. Methods: Chemokine gene expressions were assessed by reverse transcription-polymerase chain reaction, while the releases of chemokines were determined by flow cytometry or enzyme-linked immunosorbent assay (ELISA). To elucidate the intracellular signal transduction regulating the chemokine expression, phosphorylated-extracellular signal-regulated kinase (ERK), phosphorylated-p38 mitogen-activated protein kinase (MAPK) and nuclear translocated nuclear factor (NF)-κB-DNA binding were quantitatively assessed by ELISA. Results: Either SCF or TNF-α could induce release from HMC-1 cells of interleukin (IL)-8, monocyte chemoattractant protein (MCP)-1, regulated upon activation normal T-cell expressed and secreted (RANTES), and I-309, while SCF and TNF-α induced release of macrophage inflammatory protein (MIP)-1β and interferon-γ-inducible protein-10 (IP-10), respectively. Using various selective inhibitors for signaling molecules, we found that the inductions of IL-8, MCP-1, and I-309 were mediated by either SCF-activated ERK or TNF-α-activated p38 MAPK, while the induction of IP-10 by TNF-α was mediated by both activated p38 MAPK and NF-κB. The induction of RANTES by SCF or TNF-α was mediated by ERK and NF-κB, respectively, and SCF induced MIP-1β release was mediated by ERK. Conclusion: The above results therefore elucidated the different intracellular signaling pathways regulating the release of different chemokines from SCF and TNF-α-activated mast cells, thereby shedding light for the immunopathological mechanisms of mast cell-mediated diseases. Copyright © Blackwell Munksgaard 2006.-
dc.languageeng-
dc.relation.ispartofAllergy: European Journal of Allergy and Clinical Immunology-
dc.subjectBasic mechanisms-
dc.subjectChemokines-
dc.subjectMast cells-
dc.titleMolecular mechanisms for the release of chemokines from human leukemic mast cell line (HMC)-1 cells activated by SCF and TNF-α: Roles of ERK, p38 MAPK, and NF-κB-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1398-9995.2006.00972.x-
dc.identifier.pmid16436136-
dc.identifier.scopuseid_2-s2.0-33644980666-
dc.identifier.volume61-
dc.identifier.issue3-
dc.identifier.spage289-
dc.identifier.epage297-
dc.identifier.eissn1398-9995-
dc.identifier.isiWOS:000234853900004-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats