TY - JOUR
T1 - The novel heart-specific RING finger protein 207 is involved in energy metabolism in cardiomyocytes
AU - Mizushima, Wataru
AU - Takahashi, Hidehisa
AU - Watanabe, Masashi
AU - Kinugawa, Shintaro
AU - Matsushima, Shouji
AU - Takada, Shingo
AU - Yokota, Takashi
AU - Furihata, Takaaki
AU - Matsumoto, Junichi
AU - Tsuda, Masaya
AU - Chiba, Ikuru
AU - Nagashima, Shun
AU - Yanagi, Shigeru
AU - Matsumoto, Masaki
AU - Nakayama, Keiichi I.
AU - Tsutsui, Hiroyuki
AU - Hatakeyama, Shigetsugu
N1 - Funding Information:
This work was supported in part by KAKENHI (24112006, 15H04690) from the Ministry of Education, Culture, Sports, Science and Technology in Japan and by Japan Diabetes Foundation and the Uehara Memorial Foundation (to S. Hatakeyama).
Publisher Copyright:
© 2016 Elsevier Ltd
PY - 2016/11/1
Y1 - 2016/11/1
N2 - 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.
AB - 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.
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U2 - 10.1016/j.yjmcc.2016.09.013
DO - 10.1016/j.yjmcc.2016.09.013
M3 - Article
C2 - 27677939
AN - SCOPUS:84989318332
SN - 0022-2828
VL - 100
SP - 43
EP - 53
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
ER -