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Knockdown of Sestrin2 Increases Lipopolysaccharide-Induced Oxidative Stress, Apoptosis, and Fibrotic Reactions in H9c2 Cells and Heart Tissues of Mice via an AMPK-Dependent Mechanism
Joint Authors
Baik, Sei Hyun
Chung, Hye Soo
Yoo, Hye Jin
Seo, Ji-A
Kim, Sin Gon
Kim, Nan Hee
Choi, Kyung Mook
Hwang, Hwan-Jin
Kim, Joo Won
Source
Issue
Vol. 2018, Issue 2018 (31 Dec. 2018), pp.1-10, 10 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2018-07-05
Country of Publication
Egypt
No. of Pages
10
Main Subjects
Abstract EN
Sestrin2 (sesn2) is an endogenous antioxidant protein that has recently gained attention for its potential to treat various inflammatory diseases.
However, the relationship of sesn2 with cardiomyopathy is still unclear.
In H9c2 cells, sesn2 knockdown reduced the level of 5′ adenosine monophosphate-activated protein kinase (AMPK) phosphorylation, downregulated antioxidant genes including catalase and superoxide dismutase (SOD2), and increased reactive oxygen species (ROS) production upon lipopolysaccharide (LPS) treatment.
LPS-mediated cell death and the expression of matrix metalloproteinase (MMP) 2 and MMP9 were significantly increased by sesn2 knockdown.
However, these increases were prevented by treatment with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), an AMPK activator.
Consistent with the in vitro results, AMPK phosphorylation was decreased in heart tissue from sesn2 knockdown mice compared to heart tissue from control C57BL/6 mice, which was associated with decreased expression of antioxidant genes and increased LPS-mediated cell death signaling.
Furthermore, the decrease in AMPK phosphorylation caused by sesn2 knockdown increased LPS-mediated expression of cardiac fibrotic factors, including collagen type I and type III, in addition to MMP2 and MMP9, in heart tissue from C57BL/6 mice.
These results suggest that sesn2 is a novel potential therapeutic target for cardiomyopathy under inflammatory conditions.
American Psychological Association (APA)
Hwang, Hwan-Jin& Kim, Joo Won& Chung, Hye Soo& Seo, Ji-A& Kim, Sin Gon& Kim, Nan Hee…[et al.]. 2018. Knockdown of Sestrin2 Increases Lipopolysaccharide-Induced Oxidative Stress, Apoptosis, and Fibrotic Reactions in H9c2 Cells and Heart Tissues of Mice via an AMPK-Dependent Mechanism. Mediators of Inflammation،Vol. 2018, no. 2018, pp.1-10.
https://search.emarefa.net/detail/BIM-1203999
Modern Language Association (MLA)
Hwang, Hwan-Jin…[et al.]. Knockdown of Sestrin2 Increases Lipopolysaccharide-Induced Oxidative Stress, Apoptosis, and Fibrotic Reactions in H9c2 Cells and Heart Tissues of Mice via an AMPK-Dependent Mechanism. Mediators of Inflammation No. 2018 (2018), pp.1-10.
https://search.emarefa.net/detail/BIM-1203999
American Medical Association (AMA)
Hwang, Hwan-Jin& Kim, Joo Won& Chung, Hye Soo& Seo, Ji-A& Kim, Sin Gon& Kim, Nan Hee…[et al.]. Knockdown of Sestrin2 Increases Lipopolysaccharide-Induced Oxidative Stress, Apoptosis, and Fibrotic Reactions in H9c2 Cells and Heart Tissues of Mice via an AMPK-Dependent Mechanism. Mediators of Inflammation. 2018. Vol. 2018, no. 2018, pp.1-10.
https://search.emarefa.net/detail/BIM-1203999
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1203999