Nanostructured, Self-Assembling Peptide K5 Blocks TNF-alpha and PGE(2) Production by Suppression of the AP-1/p38 Pathway
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yang, Woo Seok | - |
dc.contributor.author | Park, Yung Chul | - |
dc.contributor.author | Kim, Ji Hye | - |
dc.contributor.author | Kim, Hye Ri | - |
dc.contributor.author | Yu, Tao | - |
dc.contributor.author | Byeon, Se Eun | - |
dc.contributor.author | Unsworth, Larry D. | - |
dc.contributor.author | Lee, Jaehwi | - |
dc.contributor.author | Cho, Jae Youl | - |
dc.date.available | 2019-05-29T09:35:59Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 0962-9351 | - |
dc.identifier.issn | 1466-1861 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/20947 | - |
dc.description.abstract | Nanostructured, self-assembling peptides hold promise for a variety of regenerative medical applications such as 3D cell culture systems, accelerated wound healing, and nerve repair. The aim of this study was to determine whether the self-assembling peptide K5 can be applied as a carrier of anti-inflammatory drugs. First, we examined whether the K5 self-assembling peptide itself can modulate various cellular inflammatory responses. We found that peptide K5 significantly suppressed the release of tumor-necrosis-factor-(TNF-) alpha and prostaglandin E-2 (PGE(2)) from RAW264.7 cells and peritoneal macrophages stimulated by lipopolysaccharide (LPS). Similarly, there was inhibition of cyclooxygenase- (COX-) 2 mRNA expression assessed by real-time PCR, indicating that the inhibition is at the transcriptional level. In agreement with this finding, peptide K5 suppressed the translocation of the transcription factors activator protein (AP-1) and c-Jun and inhibited upstream inflammatory effectors including mitogen activated protein kinase (MAPK), p38, and mitogen-activated protein kinase kinase 3/6 (MKK 3/6). Whether this peptide exerts its effects via a transmembrane or cytoplasmic receptor is not clear. However, our data strongly suggest that the nanostructured, self-assembling peptide K5 may possess significant anti-inflammatory activity via suppression of the p38/AP-1 pathway. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | HINDAWI LTD | - |
dc.title | Nanostructured, Self-Assembling Peptide K5 Blocks TNF-alpha and PGE(2) Production by Suppression of the AP-1/p38 Pathway | - |
dc.type | Article | - |
dc.identifier.doi | 10.1155/2012/489810 | - |
dc.identifier.bibliographicCitation | MEDIATORS OF INFLAMMATION, v.2012 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000301414300001 | - |
dc.identifier.scopusid | 2-s2.0-84858142404 | - |
dc.citation.title | MEDIATORS OF INFLAMMATION | - |
dc.citation.volume | 2012 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordPlus | TOLL-LIKE RECEPTORS | - |
dc.subject.keywordPlus | RHEUMATOID-ARTHRITIS | - |
dc.subject.keywordPlus | NANOFIBER SCAFFOLDS | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | T-CELLS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | LIPOPOLYSACCHARIDE | - |
dc.subject.keywordPlus | MACROPHAGES | - |
dc.subject.keywordPlus | RELEASE | - |
dc.subject.keywordPlus | GINSENG | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.