Arginase inhibition restores endothelial function in diet-induced obesity
DC Field | Value | Language |
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dc.contributor.author | Chung, Ji Hyung | - |
dc.contributor.author | Moon, Jiyoung | - |
dc.contributor.author | Lee, Youn Sue | - |
dc.contributor.author | Chung, Hye-Kyung | - |
dc.contributor.author | Lee, Seung-Min | - |
dc.contributor.author | Shin, Min-Jeong | - |
dc.date.accessioned | 2021-09-05T06:06:13Z | - |
dc.date.available | 2021-09-05T06:06:13Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2014-08-22 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/97666 | - |
dc.description.abstract | Arginase may play a major role in the regulation of vascular function in various cardiovascular disorders by impairing nitric oxide (NO) production. In the current study, we investigated whether supplementation of the arginase inhibitor N-omega-hydroxy-nor-L-arginine (nor-NOHA) could restore endothelial function in an animal model of diet-induced obesity. Arginase 1 expression was significantly lower in the aorta of C57BL/6J mice fed a high-fat diet (HFD) supplemented with nor-NOHA (40 mg kg(-1)/day) than in mice fed HFD without nor-NOHA. Arginase inhibition led to considerable increases in eNOS expression and NO levels and significant decreases in the levels of circulating ICAM-1. These findings were further confirmed by the results of siRNA-mediated knockdown of Arg in human umbilical vein endothelial cells. In conclusion, arginase inhibition can help restore dysregulated endothelial function by increasing the eNOS-dependent NO production in the endothelium, indicating that arginase could be a therapeutic target for correcting obesity-induced vascular endothelial dysfunction. (C) 2014 Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.subject | OXIDE-MEDIATED DILATION | - |
dc.subject | NITRIC-OXIDE | - |
dc.subject | ISCHEMIA-REPERFUSION | - |
dc.subject | CORONARY ARTERIOLES | - |
dc.subject | VASCULAR ARGINASE | - |
dc.subject | DYSFUNCTION | - |
dc.subject | HYPERTENSION | - |
dc.subject | ARGININE | - |
dc.subject | NO | - |
dc.subject | HYPERCHOLESTEROLEMIA | - |
dc.title | Arginase inhibition restores endothelial function in diet-induced obesity | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Shin, Min-Jeong | - |
dc.identifier.doi | 10.1016/j.bbrc.2014.07.083 | - |
dc.identifier.scopusid | 2-s2.0-84906934587 | - |
dc.identifier.wosid | 000348743200003 | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.451, no.2, pp.179 - 183 | - |
dc.relation.isPartOf | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.title | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.volume | 451 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 179 | - |
dc.citation.endPage | 183 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.subject.keywordPlus | OXIDE-MEDIATED DILATION | - |
dc.subject.keywordPlus | NITRIC-OXIDE | - |
dc.subject.keywordPlus | ISCHEMIA-REPERFUSION | - |
dc.subject.keywordPlus | CORONARY ARTERIOLES | - |
dc.subject.keywordPlus | VASCULAR ARGINASE | - |
dc.subject.keywordPlus | DYSFUNCTION | - |
dc.subject.keywordPlus | HYPERTENSION | - |
dc.subject.keywordPlus | ARGININE | - |
dc.subject.keywordPlus | NO | - |
dc.subject.keywordPlus | HYPERCHOLESTEROLEMIA | - |
dc.subject.keywordAuthor | Arginase | - |
dc.subject.keywordAuthor | Endothelial function | - |
dc.subject.keywordAuthor | Nitric oxide | - |
dc.subject.keywordAuthor | Obesity | - |
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