Expression and function of semaphorin 3A and its receptors in human monocyte-derived macrophages
DC Field | Value | Language |
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dc.contributor.author | Ji, Jong-Dae | - |
dc.contributor.author | Park-Min, Kyung-Hyun | - |
dc.contributor.author | Ivashkiv, Lionel B. | - |
dc.date.accessioned | 2021-09-08T18:32:01Z | - |
dc.date.available | 2021-09-08T18:32:01Z | - |
dc.date.created | 2021-06-10 | - |
dc.date.issued | 2009-04 | - |
dc.identifier.issn | 0198-8859 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/120348 | - |
dc.description.abstract | Semaphorins are a large family of secreted and membrane-bound proteins. Recently, several roles of semaphorins in the immune system have emerged. Several semaphorins and their receptors are expressed in a variety of lymphoid and myeloid cells and affect immune cell functions, including cell proliferation, differentiation, chemotaxis, and cytokine production. However, the roles of class 3 semaphorins in human myeloid cells are not well known. Here we examined the regulation of expression of class 3 semaphorins and their receptors by inflammatory stimuli and their function in human macrophages. We show that the expression of Sema3A receptors (neuropilin-1 (NRP-1), NRP-2, plexin A1, plexin A2, and plexin A3) significantly increased during M-CSF-mediated differentiation of monocytes into macrophages under conditions that promote an M2 alternatively activated macrophage phenotype. Consistent with increased NRP-1 expression, cell surface binding of Senna3A increased during M2 differentiation. Interferon (IFN)-gamma and lipopolysaccharide, which promote classical M1 macrophage activation affected expression of NRP-1, NRP-2 and plexin A1. IFN-gamma decreased NRP-1 expression and LPS suppressed NRP-2 and plexin A1 expression. Furthermore we show that Sema3A induced apoptosis in monocyte-derived macrophages and cooperated with anti-Fas CH11 antibody to augment apoptosis. Our results suggest that Sema3A plays a role in induction of apoptosis in monocyte-derived macrophages that are resistant to Fas-induced apoptosis, and that its function can be modulated in inflammatory conditions. (C) 2009 Society. Published by Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER SCIENCE INC | - |
dc.subject | CELLS | - |
dc.subject | NEUROPILIN-1 | - |
dc.subject | ACTIVATION | - |
dc.subject | APOPTOSIS | - |
dc.subject | REORGANIZATION | - |
dc.subject | CYTOSKELETON | - |
dc.subject | INHIBITION | - |
dc.subject | INDUCTION | - |
dc.subject | RESPONSES | - |
dc.subject | GROWTH | - |
dc.title | Expression and function of semaphorin 3A and its receptors in human monocyte-derived macrophages | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Ji, Jong-Dae | - |
dc.identifier.doi | 10.1016/j.humimm.2009.01.026 | - |
dc.identifier.scopusid | 2-s2.0-62949121736 | - |
dc.identifier.wosid | 000265133900001 | - |
dc.identifier.bibliographicCitation | HUMAN IMMUNOLOGY, v.70, no.4, pp.211 - 217 | - |
dc.relation.isPartOf | HUMAN IMMUNOLOGY | - |
dc.citation.title | HUMAN IMMUNOLOGY | - |
dc.citation.volume | 70 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 211 | - |
dc.citation.endPage | 217 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | NEUROPILIN-1 | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | REORGANIZATION | - |
dc.subject.keywordPlus | CYTOSKELETON | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | RESPONSES | - |
dc.subject.keywordPlus | GROWTH | - |
dc.subject.keywordAuthor | Semaphorin | - |
dc.subject.keywordAuthor | Neuropilin | - |
dc.subject.keywordAuthor | Plexin | - |
dc.subject.keywordAuthor | Macrophages | - |
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