Anti-inflammatory effects of 9-cis-retinoic acid on beta-amyloid treated human microglial cells
DC Field | Value | Language |
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dc.contributor.author | Sanjay | - |
dc.contributor.author | Kim, Jae Young | - |
dc.date.accessioned | 2023-03-14T07:40:58Z | - |
dc.date.available | 2023-03-14T07:40:58Z | - |
dc.date.created | 2023-03-10 | - |
dc.date.issued | 2022-12 | - |
dc.identifier.issn | 1721-727X | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/87122 | - |
dc.description.abstract | Objective: Alzheimer's disease (AD) is a neurodegenerative disease that abolishes cognitive and analytical abilities to perform basic day-to-day tasks. Microglia are involved in AD-associated neuroinflammation in response to amyloid beta-peptide (A beta). This study focused on observing the immunomodulatory effects of 9-cis-retinoic acid (9-Cis-RA) the active metabolite of vitamin A, on A beta-treated human microglial HMO6 cells. Methods: HMO6 cells were treated with A beta 42 in the absence or presence of 9-cis-RA, and the expression of M1-and M2-associated molecules, Toll like receptors (TLRs), and triggering receptor expressed on myeloid cells 2 (TREM2) were examined. Results: The levels of M1-markers [cluster of differentiation (CD86) and inducible nitric oxide synthase (iNOS)] and -cytokines [tumor necrosis factor (TNF-alpha), interleukin (IL)-6, and IL-1 beta], inflammatory receptors (TLR2 and TLR4), and reactive oxygen species increased significantly in A beta-treated HMO6 cells. In contrast, the levels of M2-markers (CD206 and arginase-1) and -cytokines (IL-10, IL-4, and C-C motif chemokine ligand 17) the anti-inflammatory receptor TLR10 was significantly suppressed. However, 9-cis-RA treatment reversed the A beta-induced upregulation of expression of M1-associated molecules and upregulated the expression of M2-associated molecules. Moreover, 9-cis-RA treatment augmented A beta uptake by HMO6 cells, possibly by increasing the cell surface protein levels of TREM2, which is a receptor of A beta that promotes A beta phagocytosis by microglia. Conclusion: Our results suggest that 9-cis-RA is a potential therapeutic agent for AD. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | SAGE PUBLICATIONS INC | - |
dc.relation.isPartOf | EUROPEAN JOURNAL OF INFLAMMATION | - |
dc.title | Anti-inflammatory effects of 9-cis-retinoic acid on beta-amyloid treated human microglial cells | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000928050800001 | - |
dc.identifier.doi | 10.1177/1721727X221143651 | - |
dc.identifier.bibliographicCitation | EUROPEAN JOURNAL OF INFLAMMATION, v.20 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.scopusid | 2-s2.0-85143140960 | - |
dc.citation.title | EUROPEAN JOURNAL OF INFLAMMATION | - |
dc.citation.volume | 20 | - |
dc.contributor.affiliatedAuthor | Sanjay | - |
dc.contributor.affiliatedAuthor | Kim, Jae Young | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Alzheimer&apos | - |
dc.subject.keywordAuthor | s disease | - |
dc.subject.keywordAuthor | neuroinflammation | - |
dc.subject.keywordAuthor | 9-cis-retinoic acid | - |
dc.subject.keywordAuthor | toll like receptors | - |
dc.subject.keywordAuthor | anti-inflammation | - |
dc.subject.keywordAuthor | TREM2 | - |
dc.subject.keywordPlus | RETINOIC ACID | - |
dc.subject.keywordPlus | ALZHEIMERS-DISEASE | - |
dc.subject.keywordPlus | TRANSGENIC MICE | - |
dc.subject.keywordPlus | VITAMIN-A | - |
dc.subject.keywordPlus | POLARIZATION | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | PEPTIDES | - |
dc.subject.keywordPlus | TLR10 | - |
dc.subject.keywordPlus | IMPAIRMENT | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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