Carbon monoxide regulates glycolysis-dependent NLRP3 inflammasome activation in macrophages
DC Field | Value | Language |
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dc.contributor.author | Lee, Do Won | - |
dc.contributor.author | Shin, Ha Young | - |
dc.contributor.author | Jeong, Ji Hun | - |
dc.contributor.author | Han, Jaeseok | - |
dc.contributor.author | Ryu, Seongho | - |
dc.contributor.author | Nakahira, Kiichi | - |
dc.contributor.author | Moon, Jong-Seok | - |
dc.date.accessioned | 2021-08-11T14:23:54Z | - |
dc.date.available | 2021-08-11T14:23:54Z | - |
dc.date.issued | 2017-11-18 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.issn | 1090-2104 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/7042 | - |
dc.description.abstract | Low dose of carbon monoxide (CO) has anti-inflammatory role through various signaling pathways. Cellular metabolism has been implicated in the activation of inflammation in immune cells. However, the mechanisms by which CO-dependent metabolic regulation affect the immune response remain unclear. Here we show that CO-dependent metabolic pathway regulates the activation of the nucleotide-binding domain, leucine-rich-repeat-containing receptor (NLR), pyrin-domain-containing 3 (NLRP3) inflammasome. CO-releasing molecule-3 (CORM-3) resulted in reduced glycolysis-dependent NLRP3 inflammasome activation in macrophages. The reduced mTORC1 activation by CORM-3 resulted in less glycolysis during NLRP3 inflammasome activation. CORM-3 suppressed caspase-1 activation and the secretion of interleukin (IL)-1 beta and IL-18 in macrophages in response to lipopolysaccharide (LPS) and ATP. Moreover, CORM-3 inhibits the oligomerization of the adaptor protein apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), which is required for NLRP3-dependent caspase-1 activation. Furthermore, CORM-3-treated mice showed substantial reduction in IL-1 beta production by hyperglycemia in a mouse model of streptozotocin (STZ)-induced diabetes. Our results suggest that CO regulates glycolysis-dependent NLRP3 inflammasome activation and may provide a therapeutic approach for inflammation in metabolic diseases. (C) 2017 Elsevier Inc. All rights reserved. | - |
dc.format.extent | 7 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Academic Press | - |
dc.title | Carbon monoxide regulates glycolysis-dependent NLRP3 inflammasome activation in macrophages | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1016/j.bbrc.2017.09.111 | - |
dc.identifier.scopusid | 2-s2.0-85029741512 | - |
dc.identifier.wosid | 000413797200014 | - |
dc.identifier.bibliographicCitation | Biochemical and Biophysical Research Communications, v.493, no.2, pp 957 - 963 | - |
dc.citation.title | Biochemical and Biophysical Research Communications | - |
dc.citation.volume | 493 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 957 | - |
dc.citation.endPage | 963 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.subject.keywordPlus | SIGNALING PATHWAYS | - |
dc.subject.keywordPlus | CELL-ACTIVATION | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | GROWTH | - |
dc.subject.keywordPlus | HYPERGLYCEMIA | - |
dc.subject.keywordPlus | CASPASE-1 | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | DISEASE | - |
dc.subject.keywordPlus | COMPLEX | - |
dc.subject.keywordPlus | GLUCOSE | - |
dc.subject.keywordAuthor | CO | - |
dc.subject.keywordAuthor | Glycolysis | - |
dc.subject.keywordAuthor | NLRP3 inflammasome | - |
dc.subject.keywordAuthor | Macrophages | - |
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