Full metadata record
DC Field | Value | Language |
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dc.citation.number | 1 | - |
dc.citation.startPage | 6647 | - |
dc.citation.title | NATURE COMMUNICATIONS | - |
dc.citation.volume | 13 | - |
dc.contributor.author | Kim, Tae Kyeong | - |
dc.contributor.author | Jeon, Sejin | - |
dc.contributor.author | Park, Seonjun | - |
dc.contributor.author | Sonn, Seong-Keun | - |
dc.contributor.author | Seo, Seungwoon | - |
dc.contributor.author | Suh, Joowon | - |
dc.contributor.author | Jin, Jing | - |
dc.contributor.author | Kweon, Hyae Yon | - |
dc.contributor.author | Kim, Sinai | - |
dc.contributor.author | Moon, Shin Hye | - |
dc.contributor.author | Kweon, Okhee | - |
dc.contributor.author | Koo, Bon-Hyeock | - |
dc.contributor.author | Kim, Nayoung | - |
dc.contributor.author | Lee, Hae-Ock | - |
dc.contributor.author | Kim, Young-Myeong | - |
dc.contributor.author | Kim, Young-Joon | - |
dc.contributor.author | Park, Sung Ho | - |
dc.contributor.author | Oh, Goo Taeg | - |
dc.date.accessioned | 2023-12-21T13:18:19Z | - |
dc.date.available | 2023-12-21T13:18:19Z | - |
dc.date.created | 2022-12-27 | - |
dc.date.issued | 2022-11 | - |
dc.description.abstract | Maintaining optimal eNOS levels is important during cardiovascular events, although little is known regarding the mechanism of eNOS protection. Here, the authors show a regulatory role of endothelial OASL1 in maintaining eNOS mRNA stability and vascular biology under atheroprone conditions. Endothelial nitric oxide synthase (eNOS) decreases following inflammatory stimulation. As a master regulator of endothelial homeostasis, maintaining optimal eNOS levels is important during cardiovascular events. However, little is known regarding the mechanism of eNOS protection. In this study, we demonstrate a regulatory role for endothelial expression of 2 '-5 ' oligoadenylate synthetase-like 1 (OASL1) in maintaining eNOS mRNA stability during athero-prone conditions and consider its clinical implications. A lack of endothelial Oasl1 accelerated plaque progression, which was preceded by endothelial dysfunction, elevated vascular inflammation, and decreased NO bioavailability following impaired eNOS expression. Mechanistically, knockdown of PI3K/Akt signaling-dependent OASL expression increased Erk1/2 and NF-kappa B activation and decreased NOS3 (gene name for eNOS) mRNA expression through upregulation of the negative regulatory, miR-584, whereas a miR-584 inhibitor rescued the effects of OASL knockdown. These results suggest that OASL1/OASL regulates endothelial biology by protecting NOS3 mRNA and targeting miR-584 represents a rational therapeutic strategy for eNOS maintenance in vascular disease. | - |
dc.identifier.bibliographicCitation | NATURE COMMUNICATIONS, v.13, no.1, pp.6647 | - |
dc.identifier.doi | 10.1038/s41467-022-34433-z | - |
dc.identifier.issn | 2041-1723 | - |
dc.identifier.scopusid | 2-s2.0-85141191733 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/60471 | - |
dc.identifier.wosid | 000879110700018 | - |
dc.language | 영어 | - |
dc.publisher | NATURE PORTFOLIO | - |
dc.title | 2 '-5 ' oligoadenylate synthetase-like 1 (OASL1) protects against atherosclerosis by maintaining endothelial nitric oxide synthase mRNA stability | - |
dc.type | Article | - |
dc.description.isOpenAccess | TRUE | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | DOWN-REGULATION | - |
dc.subject.keywordPlus | PATHOGENESIS | - |
dc.subject.keywordPlus | DYSFUNCTION | - |
dc.subject.keywordPlus | DEFICIENCY | - |
dc.subject.keywordPlus | PROMOTES | - |
dc.subject.keywordPlus | TRANSCRIPTION | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | DISEASE | - |
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