Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes
- Authors
- Kim, Nami; Jung, Youngae; Nam, Miso; Kang, Mi Sun; Lee, Min Kyung; Cho, Youngjin; Choi, Eue-Keun; Hwang, Geum-Sook; Kim, Hyeon Soo
- Issue Date
- 4-9월-2017
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- SCIENTIFIC REPORTS, v.7
- Indexed
- SCIE
SCOPUS
- Journal Title
- SCIENTIFIC REPORTS
- Volume
- 7
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/82272
- DOI
- 10.1038/s41598-017-09675-3
- ISSN
- 2045-2322
- 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.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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