Chemokine receptor 5 blockade modulates macrophage trafficking in renal ischaemic-reperfusion injury
DC Field | Value | Language |
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dc.contributor.author | Yoo, Kyung Don | - |
dc.contributor.author | Cha, Ran-hui | - |
dc.contributor.author | Lee, Sunhwa | - |
dc.contributor.author | Kim, Ji Eun | - |
dc.contributor.author | Kim, Kyu Hong | - |
dc.contributor.author | Lee, Jong Soo | - |
dc.contributor.author | Kim, Dong Ki | - |
dc.contributor.author | Kim, Yon Su | - |
dc.contributor.author | Yang, Seung Hee | - |
dc.date.available | 2020-11-10T06:48:35Z | - |
dc.date.issued | 2020-05 | - |
dc.identifier.issn | 1582-1838 | - |
dc.identifier.issn | 1582-4934 | - |
dc.identifier.uri | https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/28153 | - |
dc.description.abstract | Chemokine receptor 5 (CCR5) is a pivotal regulator of macrophage trafficking in the kidneys in response to an inflammatory cascade. We investigated the role of CCR5 in experimental ischaemic-reperfusion injury (IRI) pathogenesis. To establish IRI, we clamped the bilateral renal artery pedicle for 30 min and then reperfused the kidney. We performed adoptive transfer of lipopolysaccharide (LPS)-treated RAW 264.7 macrophages following macrophage depletion in mice. B6.CCR5(-/-) mice showed less severe IRI based on tubular epithelial cell apoptosis than did wild-type mice. CXCR3 expression in CD11b(+) cells and inducible nitric oxide synthase levels were more attenuated in B6.CCR5(-/-) mice. B6.CCR5(-/-) mice showed increased arginase-1 and CD206 expression. Macrophage-depleted wild-type mice showed more injury than B6.CCR5(-/-) mice after M1 macrophage transfer. Adoptive transfer of LPS-treated RAW 264.7 macrophages reversed the protection against IRI in wild-type, but not B6.CCR5(-/-) mice. Upon knocking out CCR5 in macrophages, migration of bone marrow-derived macrophages from wild-type mice towards primary tubular epithelial cells with recombinant CCR5 increased. Phospho-CCR5 expression in renal tissues of patients with acute tubular necrosis was increased, showing a positive correlation with tubular inflammation. In conclusion, CCR5 deficiency favours M2 macrophage activation, and blocking CCR5 might aid in treating acute kidney injury. | - |
dc.format.extent | 13 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | WILEY | - |
dc.title | Chemokine receptor 5 blockade modulates macrophage trafficking in renal ischaemic-reperfusion injury | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1111/jcmm.15207 | - |
dc.identifier.scopusid | 2-s2.0-85082528849 | - |
dc.identifier.wosid | 000522303100001 | - |
dc.identifier.bibliographicCitation | Journal of Cellular and Molecular Medicine, v.24, no.10, pp 5515 - 5527 | - |
dc.citation.title | Journal of Cellular and Molecular Medicine | - |
dc.citation.volume | 24 | - |
dc.citation.number | 10 | - |
dc.citation.startPage | 5515 | - |
dc.citation.endPage | 5527 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Research & Experimental Medicine | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Medicine, Research & Experimental | - |
dc.subject.keywordPlus | T-CELLS | - |
dc.subject.keywordPlus | PATHOPHYSIOLOGICAL ROLE | - |
dc.subject.keywordPlus | KIDNEY | - |
dc.subject.keywordPlus | CCR5 | - |
dc.subject.keywordPlus | INFILTRATION | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | CONTRIBUTE | - |
dc.subject.keywordPlus | FIBROSIS | - |
dc.subject.keywordPlus | HYPOXIA | - |
dc.subject.keywordPlus | CXCR3 | - |
dc.subject.keywordAuthor | acute kidney injury | - |
dc.subject.keywordAuthor | bilateral ischaemia-reperfusion injury | - |
dc.subject.keywordAuthor | CC chemokine receptor 5 | - |
dc.subject.keywordAuthor | chemokine | - |
dc.subject.keywordAuthor | macrophage | - |
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