| Pro-inflammatory cytokines induce suppressor of cytokine signaling-3 in human periodontal ligament cells. | |
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MedLine Citation:
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PMID: 20478455 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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INTRODUCTION: Periapical inflammation is initiated by insult to the dental pulp and mediated by inflammatory cytokines in the periodontal tissue. On the other hand, the destruction of tissue can be prevented by the suppression of pro-inflammatory cytokine activity. The balance between these cytokines and their counterregulatory molecules has been suggested to regulate tissue destruction. Suppressors of cytokine signaling (SOCS) proteins are known to suppress inflammatory cytokine signaling via the classic negative feedback loop. However, the mechanism by which they are induced by inflammatory cytokines and regulated during the development of periodontal disease remains to be clarified. We investigated the effects of inflammatory cytokines on SOCS protein expression and their signaling pathways in human periodontal ligament (PDL) cells. METHODS: We examined the effect of inflammatory cytokines on SOCSs expression and its signaling pathway in human PDL cells using reverse transcription- and real-time polymerase chain reaction, Western blot methods. Furthermore, we also examined whether these cytokines-induced SOCS-3 suppress chemokines secretion using ELISA methods. RESULTS: We found that inflammatory cytokines interleukin (IL)-1beta and IL-6 induced expression of SOCS-3 but not that of SOCS-2 in human PDL cells. IL-1beta and IL-6 simultaneously induced IL-8 and monocyte chemoattractant protein-1 secretion in PDL cells, whereas SOCS-3 overexpression suppressed secretion of these chemokines through inhibition of phosphorylation in downstream signaling. CONCLUSION: The results suggest that pro-inflammatory cytokines induced SOCS-3 expression. The SOCS-3 induction suggests playing an important role in negative feedback, suppressing serious destruction of periodontal tissue in apical periodontitis through a chemokine-dependent mechanism. |
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Authors:
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Akie Fukushima; Hiroshi Kajiya; Toshio Izumi; Chieko Shigeyama; Koji Okabe; Hisashi Anan |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-04-10 |
Journal Detail:
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Title: Journal of endodontics Volume: 36 ISSN: 1878-3554 ISO Abbreviation: J Endod Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-05-18 Completed Date: 2010-09-28 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7511484 Medline TA: J Endod Country: United States |
Other Details:
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Languages: eng Pagination: 1004-8 Citation Subset: D |
Copyright Information:
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Copyright 2010 American Association of Endodontists. Published by Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Odontology, Fukuoka Dental College, Fukuoka, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Blotting, Western Cells, Cultured Chemokine CCL2 / analysis, immunology Cytokines / immunology* Enzyme-Linked Immunosorbent Assay Humans Interleukin-1beta / immunology Interleukin-6 / immunology Interleukin-8 / analysis, immunology Janus Kinases / analysis, immunology Mitogen-Activated Protein Kinases / analysis, immunology Periodontal Ligament / cytology, immunology* Phosphorylation RNA, Messenger / analysis Receptors, Interleukin-6 / analysis, immunology Reverse Transcriptase Polymerase Chain Reaction STAT Transcription Factors / analysis, immunology Signal Transduction / immunology* Suppressor of Cytokine Signaling Proteins / analysis, immunology* Time Factors Up-Regulation / immunology p38 Mitogen-Activated Protein Kinases / analysis, immunology |
| Chemical | |
Reg. No./Substance:
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0/CCL2 protein, human; 0/Chemokine CCL2; 0/Cytokines; 0/Interleukin-1beta; 0/Interleukin-6; 0/Interleukin-8; 0/RNA, Messenger; 0/Receptors, Interleukin-6; 0/SOCS2 protein, human; 0/SOCS3 protein, human; 0/STAT Transcription Factors; 0/Suppressor of Cytokine Signaling Proteins; EC 2.7.10.2/Janus Kinases; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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