Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 오구택 | * |
dc.contributor.author | 전세진 | * |
dc.contributor.author | 서주원 | * |
dc.date.accessioned | 2023-01-04T16:31:07Z | - |
dc.date.available | 2023-01-04T16:31:07Z | - |
dc.date.issued | 2022 | * |
dc.identifier.issn | 2041-1723 | * |
dc.identifier.other | OAK-32607 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/262980 | - |
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.language | English | * |
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.relation.issue | 1 | * |
dc.relation.volume | 13 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | NATURE COMMUNICATIONS | * |
dc.identifier.doi | 10.1038/s41467-022-34433-z | * |
dc.identifier.wosid | WOS:000879110700018 | * |
dc.identifier.scopusid | 2-s2.0-85141191733 | * |
dc.author.google | Kim, Tae Kyeong | * |
dc.author.google | Jeon, Sejin | * |
dc.author.google | Park, Seonjun | * |
dc.author.google | Sonn, Seong-Keun | * |
dc.author.google | Seo, Seungwoon | * |
dc.author.google | Suh, Joowon | * |
dc.author.google | Jin, Jing | * |
dc.author.google | Kweon, Hyae Yon | * |
dc.author.google | Kim, Sinai | * |
dc.author.google | Moon, Shin Hye | * |
dc.author.google | Kweon, Okhee | * |
dc.author.google | Koo, Bon-Hyeock | * |
dc.author.google | Kim, Nayoung | * |
dc.author.google | Lee, Hae-Ock | * |
dc.author.google | Kim, Young-Myeong | * |
dc.author.google | Kim, Young-Joon | * |
dc.author.google | Park, Sung Ho | * |
dc.author.google | Oh, Goo Taeg | * |
dc.contributor.scopusid | 오구택(7007056663) | * |
dc.contributor.scopusid | 전세진(55609439300) | * |
dc.contributor.scopusid | 서주원(57215538916) | * |
dc.date.modifydate | 20240308133737 | * |