Cited 11 times in
Single-cell transcriptomics reveal cellular diversity of aortic valve and the immunomodulation by PPARγ during hyperlipidemia
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 안수진 | - |
dc.contributor.author | 이삭 | - |
dc.contributor.author | 이상학 | - |
dc.contributor.author | 이승현 | - |
dc.date.accessioned | 2023-03-10T01:35:40Z | - |
dc.date.available | 2023-03-10T01:35:40Z | - |
dc.date.issued | 2022-09 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/193251 | - |
dc.description.abstract | Valvular inflammation triggered by hyperlipidemia has been considered as an important initial process of aortic valve disease; however, cellular and molecular evidence remains unclear. Here, we assess the relationship between plasma lipids and valvular inflammation, and identify association of low-density lipoprotein with increased valvular lipid and macrophage accumulation. Single-cell RNA sequencing analysis reveals the cellular heterogeneity of leukocytes, valvular interstitial cells, and valvular endothelial cells, and their phenotypic changes during hyperlipidemia leading to recruitment of monocyte-derived MHC-IIhi macrophages. Interestingly, we find activated PPARγ pathway in Cd36+ valvular endothelial cells increased in hyperlipidemic mice, and the conservation of PPARγ activation in non-calcified human aortic valves. While the PPARγ inhibition promotes inflammation, PPARγ activation using pioglitazone reduces valvular inflammation in hyperlipidemic mice. These results show that low-density lipoprotein is the main lipoprotein accumulated in the aortic valve during hyperlipidemia, leading to early-stage aortic valve disease, and PPARγ activation protects the aortic valve against inflammation. | - |
dc.description.statementOfResponsibility | open | - |
dc.format | application/pdf | - |
dc.language | English | - |
dc.publisher | Nature Pub. Group | - |
dc.relation.isPartOf | NATURE COMMUNICATIONS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Aortic Valve / metabolism | - |
dc.subject.MESH | Aortic Valve Stenosis* | - |
dc.subject.MESH | Calcinosis* / genetics | - |
dc.subject.MESH | Cells, Cultured | - |
dc.subject.MESH | Endothelial Cells / metabolism | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Hyperlipidemias* / genetics | - |
dc.subject.MESH | Hyperlipidemias* / metabolism | - |
dc.subject.MESH | Immunomodulation | - |
dc.subject.MESH | Inflammation / genetics | - |
dc.subject.MESH | Inflammation / metabolism | - |
dc.subject.MESH | Lipoproteins, LDL / metabolism | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | PPAR gamma / genetics | - |
dc.subject.MESH | PPAR gamma / metabolism | - |
dc.subject.MESH | Pioglitazone / pharmacology | - |
dc.subject.MESH | Transcriptome | - |
dc.title | Single-cell transcriptomics reveal cellular diversity of aortic valve and the immunomodulation by PPARγ during hyperlipidemia | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Yonsei Biomedical Research Center (연세의생명연구원) | - |
dc.contributor.googleauthor | Seung Hyun Lee | - |
dc.contributor.googleauthor | Nayoung Kim | - |
dc.contributor.googleauthor | Minkyu Kim | - |
dc.contributor.googleauthor | Sang-Ho Woo | - |
dc.contributor.googleauthor | Inhee Han | - |
dc.contributor.googleauthor | Jisu Park | - |
dc.contributor.googleauthor | Kyeongdae Kim | - |
dc.contributor.googleauthor | Kyu Seong Park | - |
dc.contributor.googleauthor | Kibyeong Kim | - |
dc.contributor.googleauthor | Dahee Shim | - |
dc.contributor.googleauthor | Sang-Eun Park | - |
dc.contributor.googleauthor | Jing Yu Zhang | - |
dc.contributor.googleauthor | Du-Min Go | - |
dc.contributor.googleauthor | Dae-Yong Kim | - |
dc.contributor.googleauthor | Won Kee Yoon | - |
dc.contributor.googleauthor | Seung-Pyo Lee | - |
dc.contributor.googleauthor | Jongsuk Chung | - |
dc.contributor.googleauthor | Ki-Wook Kim | - |
dc.contributor.googleauthor | Jung Hwan Park | - |
dc.contributor.googleauthor | Seung Hyun Lee | - |
dc.contributor.googleauthor | Sak Lee | - |
dc.contributor.googleauthor | Soo-Jin Ann | - |
dc.contributor.googleauthor | Sang-Hak Lee | - |
dc.contributor.googleauthor | Hyo-Suk Ahn | - |
dc.contributor.googleauthor | Seong Cheol Jeong | - |
dc.contributor.googleauthor | Tae Kyeong Kim | - |
dc.contributor.googleauthor | Goo Taeg Oh | - |
dc.contributor.googleauthor | Woong-Yang Park | - |
dc.contributor.googleauthor | Hae-Ock Lee | - |
dc.contributor.googleauthor | Jae-Hoon Choi | - |
dc.identifier.doi | 10.1038/s41467-022-33202-2 | - |
dc.contributor.localId | A02243 | - |
dc.contributor.localId | A02807 | - |
dc.contributor.localId | A02833 | - |
dc.contributor.localId | A02935 | - |
dc.relation.journalcode | J02293 | - |
dc.identifier.eissn | 2041-1723 | - |
dc.identifier.pmid | 36115863 | - |
dc.contributor.alternativeName | Ann, Soo Jin | - |
dc.contributor.affiliatedAuthor | 안수진 | - |
dc.contributor.affiliatedAuthor | 이삭 | - |
dc.contributor.affiliatedAuthor | 이상학 | - |
dc.contributor.affiliatedAuthor | 이승현 | - |
dc.citation.volume | 13 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 5461 | - |
dc.identifier.bibliographicCitation | NATURE COMMUNICATIONS, Vol.13(1) : 5461, 2022-09 | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.