Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes

Nami Kim, Youngae Jung, Miso Nam, Mi Sun Kang, Min Kyung Lee, Youngjin Cho, Eue Keun Choi, Geum Sook Hwang, Hyeon Soo Kim

Research output: Contribution to journalArticle

6 Citations (Scopus)

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-β1 (TGF-β1) and tumor necrosis factor-α (TNF-α). 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-β1 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-β signalling pathways. Ang II concentration, along with TGF-β1 and tumor necrosis factor-α 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.

Original languageEnglish
Article number10328
JournalScientific Reports
Volume7
Issue number1
DOIs
Publication statusPublished - 2017 Dec 1

Fingerprint

AMP-Activated Protein Kinases
Angiotensin II
Muscle Cells
Inflammation
JNK Mitogen-Activated Protein Kinases
Transforming Growth Factors
Reactive Oxygen Species
Phosphorylation
Atrial Fibrillation
Tumor Necrosis Factor-alpha
Calcium
Oxygen Consumption
Cardiac Arrhythmias
Oxidative Stress

ASJC Scopus subject areas

  • General

Cite this

Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes. / Kim, Nami; Jung, Youngae; Nam, Miso; Sun Kang, Mi; Lee, Min Kyung; Cho, Youngjin; Choi, Eue Keun; Hwang, Geum Sook; Kim, Hyeon Soo.

In: Scientific Reports, Vol. 7, No. 1, 10328, 01.12.2017.

Research output: Contribution to journalArticle

Kim, Nami ; Jung, Youngae ; Nam, Miso ; Sun Kang, Mi ; Lee, Min Kyung ; Cho, Youngjin ; Choi, Eue Keun ; Hwang, Geum Sook ; Kim, Hyeon Soo. / Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes. In: Scientific Reports. 2017 ; Vol. 7, No. 1.
@article{4b8607ed73354a1bb0c10942db2a88fd,
title = "Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes",
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-β1 (TGF-β1) and tumor necrosis factor-α (TNF-α). 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-β1 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-β signalling pathways. Ang II concentration, along with TGF-β1 and tumor necrosis factor-α 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.",
author = "Nami Kim and Youngae Jung and Miso Nam and {Sun Kang}, Mi and Lee, {Min Kyung} and Youngjin Cho and Choi, {Eue Keun} and Hwang, {Geum Sook} and Kim, {Hyeon Soo}",
year = "2017",
month = "12",
day = "1",
doi = "10.1038/s41598-017-09675-3",
language = "English",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",
number = "1",

}

TY - JOUR

T1 - Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes

AU - Kim, Nami

AU - Jung, Youngae

AU - Nam, Miso

AU - Sun Kang, Mi

AU - Lee, Min Kyung

AU - Cho, Youngjin

AU - Choi, Eue Keun

AU - Hwang, Geum Sook

AU - Kim, Hyeon Soo

PY - 2017/12/1

Y1 - 2017/12/1

N2 - 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-β1 (TGF-β1) and tumor necrosis factor-α (TNF-α). 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-β1 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-β signalling pathways. Ang II concentration, along with TGF-β1 and tumor necrosis factor-α 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.

AB - 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-β1 (TGF-β1) and tumor necrosis factor-α (TNF-α). 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-β1 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-β signalling pathways. Ang II concentration, along with TGF-β1 and tumor necrosis factor-α 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.

UR - http://www.scopus.com/inward/record.url?scp=85028816615&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85028816615&partnerID=8YFLogxK

U2 - 10.1038/s41598-017-09675-3

DO - 10.1038/s41598-017-09675-3

M3 - Article

C2 - 28871102

AN - SCOPUS:85028816615

VL - 7

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

M1 - 10328

ER -