DC Field | Value | Language |
---|---|---|
dc.contributor.author | Koo, Jeung-Hyun | ko |
dc.contributor.author | Jang, Hyun-Young | ko |
dc.contributor.author | Lee, Youngyi | ko |
dc.contributor.author | Moon, Young Jae | ko |
dc.contributor.author | Bae, Eun Ju | ko |
dc.contributor.author | Yun, Seok-Kweon | ko |
dc.contributor.author | Park, Byung-Hyun | ko |
dc.date.accessioned | 2024-03-22T06:01:09Z | - |
dc.date.available | 2024-03-22T06:01:09Z | - |
dc.date.created | 2024-03-21 | - |
dc.date.issued | 2019-04 | - |
dc.identifier.citation | EXPERIMENTAL AND MOLECULAR MEDICINE, v.51, pp.1 - 10 | - |
dc.identifier.issn | 1226-3613 | - |
dc.identifier.uri | http://hdl.handle.net/10203/318723 | - |
dc.description.abstract | We recently reported that myeloid cell-expressed sirtuin 6 (Sirt6) plays a crucial role in M1 macrophage polarization and chemotaxis. Given the prominent role of macrophages during wound repair and macrophage heterogeneity, we hypothesized that a Sirt6 deficiency in myeloid cells would delay skin wound closure by affecting the phenotypes of macrophages in wounds. To address this question, a full-thickness excisional lesion was made in the dorsal skin of myeloid cell-specific Sirt6 knockout (KO) and wild-type mice. Wound closure was delayed in the KO mice, which exhibited less collagen deposition, suppressed angiogenesis, and reduced expression of wound healing-related genes compared to the wild-type mice. Using immunohistochemical, flow cytometric, and gene-expression analyses of macrophage subpopulations from wound tissue, we identified increased infiltration of M1 macrophages with a concomitant decrease in M2 macrophage numbers in the KO mice compared to the wild-type mice. Consistent with the in vivo wound closure defects observed in the KO mice, keratinocytes and fibroblasts treated with KO macrophage-derived conditioned medium migrated slower than those treated with wild-type macrophage-derived conditioned medium. An analysis of downstream signaling pathways indicated that impaired Akt signaling underlies the decreased M2 phenotypic switching in KO mice. These results suggest that a macrophage phenotypic switch induced by Sirt6 deficiency contributes to impaired wound healing in mice. | - |
dc.language | English | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.title | Myeloid cell-specific sirtuin 6 deficiency delays wound healing in mice by modulating inflammation and macrophage phenotypes | - |
dc.type | Article | - |
dc.identifier.wosid | 000467046900001 | - |
dc.identifier.scopusid | 2-s2.0-85064847113 | - |
dc.type.rims | ART | - |
dc.citation.volume | 51 | - |
dc.citation.beginningpage | 1 | - |
dc.citation.endingpage | 10 | - |
dc.citation.publicationname | EXPERIMENTAL AND MOLECULAR MEDICINE | - |
dc.identifier.doi | 10.1038/s12276-019-0248-9 | - |
dc.identifier.kciid | ART002459961 | - |
dc.contributor.localauthor | Park, Byung-Hyun | - |
dc.contributor.nonIdAuthor | Koo, Jeung-Hyun | - |
dc.contributor.nonIdAuthor | Jang, Hyun-Young | - |
dc.contributor.nonIdAuthor | Lee, Youngyi | - |
dc.contributor.nonIdAuthor | Moon, Young Jae | - |
dc.contributor.nonIdAuthor | Bae, Eun Ju | - |
dc.contributor.nonIdAuthor | Yun, Seok-Kweon | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | DEACETYLATION | - |
dc.subject.keywordPlus | OVEREXPRESSION | - |
dc.subject.keywordPlus | IMPAIRMENT | - |
dc.subject.keywordPlus | ACTIVATION | - |
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