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The novel heart-specific RING finger protein 207 is involved in energy metabolism in cardiomyocytes

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Title: The novel heart-specific RING finger protein 207 is involved in energy metabolism in cardiomyocytes
Authors: Mizushima, Wataru Browse this author
Takahashi, Hidehisa Browse this author →KAKEN DB
Watanabe, Masashi Browse this author
Kinugawa, Shintaro Browse this author →KAKEN DB
Matsushima, Shouji Browse this author
Takada, Shingo Browse this author →KAKEN DB
Yokota, Takashi Browse this author →KAKEN DB
Furihata, Takaaki Browse this author →KAKEN DB
Matsumoto, Junichi Browse this author
Tsuda, Masaya Browse this author
Chiba, Ikuru Browse this author
Nagashima, Shun Browse this author
Yanagi, Shigeru Browse this author →KAKEN DB
Matsumoto, Masaki Browse this author →KAKEN DB
Nakayama, Keiichi I. Browse this author →KAKEN DB
Tsutsui, Hiroyuki Browse this author →KAKEN DB
Hatakeyama, Shigetsugu Browse this author →KAKEN DB
Keywords: Cardiomyocyte
Energy metabolism
Heart failure
Issue Date: Nov-2016
Publisher: Elsevier
Journal Title: Journal of molecular and cellular cardiology
Volume: 100
Start Page: 43
End Page: 53
Publisher DOI: 10.1016/j.yjmcc.2016.09.013
PMID: 27677939
Abstract: A failing heart shows severe energy insufficiency, and it is presumed that this energy shortage plays a critical role in the development of cardiac dysfunction. However, little is known about the mechanisms that cause energy metabolic alterations in the failing heart. Here, we show that the novel RING-finger protein 207 (RNF207), which is specifically expressed in the heart, plays a role in cardiac energy metabolism. Depletion of RNF207 in neonatal rat cardiomyocytes (NRCs) leads to a reduced cellular concentration of adenosine triphosphate (ATP) and mitochondrial dysfunction. Consistent with this result, we observed here that the expression of RNF207 was significantly reduced in mice with common cardiac diseases including heart failure. Intriguingly, proteomic approaches revealed that RNF207 interacts with the voltage-dependent anion channel (VDAC), which is considered to be a key regulator of mitochondria function, as an RNF207-interacting protein. Our findings indicate that RNF207 is involved in ATP production by cardiomyocytes, suggesting that RNF207 plays an important role in the development of heart failure.
Rights: © 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license
Type: article (author version)
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 畠山 鎮次

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