Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes
DC Field | Value | Language |
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dc.contributor.author | Kim, Nami | - |
dc.contributor.author | Jung, Youngae | - |
dc.contributor.author | Nam, Miso | - |
dc.contributor.author | Kang, Mi Sun | - |
dc.contributor.author | Lee, Min Kyung | - |
dc.contributor.author | Cho, Youngjin | - |
dc.contributor.author | Choi, Eue-Keun | - |
dc.contributor.author | Hwang, Geum-Sook | - |
dc.contributor.author | Kim, Hyeon Soo | - |
dc.date.accessioned | 2021-09-03T01:53:40Z | - |
dc.date.available | 2021-09-03T01:53:40Z | - |
dc.date.created | 2021-06-16 | - |
dc.date.issued | 2017-09-04 | - |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/82272 | - |
dc.description.abstract | Inflammation is a common cause of cardiac arrhythmia. Angiotensin II (Ang II) is a major contributing factor in the pathogenesis of cardiac inflammation; however, its underlying molecular mechanism remains unclear. Here, we explored the effect of Ang II on inflammatory mechanisms and oxidative stress using HL-1 atrial myocytes. We showed that Ang II activated c-Jun N-terminal kinase (JNK) phosphorylation and other inflammatory markers, such as transforming growth factor-beta 1 (TGF-beta 1) and tumor necrosis factor-alpha (TNF-alpha). Ang II decreased oxygen consumption rate, which resulted in reactive oxygen species (ROS) generation and inhibition of ROS blocked Ang II-mediated JNK phosphorylation and TGF-beta 1 induction. Ang II induced the expression of its specific receptor, AT1R. Ang II-induced intracellular calcium production associated with Ang II-mediated signalling pathways. In addition, the generated ROS and calcium stimulated AMPK phosphorylation. Inhibiting AMPK blocked Ang II-mediated JNK and TGF-beta signalling pathways. Ang II concentration, along with TGF-beta 1 and tumor necrosis factor-alpha levels, was slightly increased in plasma of patients with atrial fibrillation. Taken together, these results suggest that Ang II induces inflammation mechanisms through an AMPK-related signalling pathway. Our results provide new molecular targets for the development of therapeutics for inflammation-related conditions, such as atrial fibrillation. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.subject | ACTIVATED PROTEIN-KINASE | - |
dc.subject | SPECIES-MEDIATED ACTIVATION | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | GLUCOSE-UPTAKE | - |
dc.subject | POTENTIAL ROLE | - |
dc.subject | MUSCLE-CELLS | - |
dc.subject | FIBRILLATION | - |
dc.subject | SYSTEM | - |
dc.subject | HEART | - |
dc.subject | EXPRESSION | - |
dc.title | Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Hyeon Soo | - |
dc.identifier.doi | 10.1038/s41598-017-09675-3 | - |
dc.identifier.scopusid | 2-s2.0-85028816615 | - |
dc.identifier.wosid | 000408997700027 | - |
dc.identifier.bibliographicCitation | SCIENTIFIC REPORTS, v.7 | - |
dc.relation.isPartOf | SCIENTIFIC REPORTS | - |
dc.citation.title | SCIENTIFIC REPORTS | - |
dc.citation.volume | 7 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.subject.keywordPlus | ACTIVATED PROTEIN-KINASE | - |
dc.subject.keywordPlus | SPECIES-MEDIATED ACTIVATION | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | GLUCOSE-UPTAKE | - |
dc.subject.keywordPlus | POTENTIAL ROLE | - |
dc.subject.keywordPlus | MUSCLE-CELLS | - |
dc.subject.keywordPlus | FIBRILLATION | - |
dc.subject.keywordPlus | SYSTEM | - |
dc.subject.keywordPlus | HEART | - |
dc.subject.keywordPlus | EXPRESSION | - |
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