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Your search keyword '"Lee, Jong-Kook"' showing total 11 results
Start Over Author "Lee, Jong-Kook" Journal scientific reports
11 results on '"Lee, Jong-Kook"'

8. Activation of endothelial β-catenin signaling induces heart failure

Author

Nakagawa, Akito, primary, Naito, Atsuhiko T., additional, Sumida, Tomokazu, additional, Nomura, Seitaro, additional, Shibamoto, Masato, additional, Higo, Tomoaki, additional, Okada, Katsuki, additional, Sakai, Taku, additional, Hashimoto, Akihito, additional, Kuramoto, Yuki, additional, Oka, Toru, additional, Lee, Jong-Kook, additional, Harada, Mutsuo, additional, Ueda, Kazutaka, additional, Shiojima, Ichiro, additional, Limbourg, Florian P., additional, Adams, Ralf H., additional, Noda, Tetsuo, additional, Sakata, Yasushi, additional, Akazawa, Hiroshi, additional, and Komuro, Issei, additional

Published
2016
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10. Monocyte-derived extracellular Nampt-dependent biosynthesis of NAD+ protects the heart against pressure overload

Author

Yano, Masamichi, primary, Akazawa, Hiroshi, additional, Oka, Toru, additional, Yabumoto, Chizuru, additional, Kudo-Sakamoto, Yoko, additional, Kamo, Takehiro, additional, Shimizu, Yu, additional, Yagi, Hiroki, additional, Naito, Atsuhiko T., additional, Lee, Jong-Kook, additional, Suzuki, Jun-ichi, additional, Sakata, Yasushi, additional, and Komuro, Issei, additional

Published
2015
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11. Monocyte-derived extracellular Nampt-dependent biosynthesis of NAD+ protects the heart against pressure overload.

Author

Yano, Masamichi, Akazawa, Hiroshi, Oka, Toru, Yabumoto, Chizuru, Kudo-Sakamoto, Yoko, Kamo, Takehiro, Shimizu, Yu, Yagi, Hiroki, Naito, Atsuhiko T., Lee, Jong-Kook, Suzuki, Jun-ichi, Sakata, Yasushi, and Komuro, Issei

Subjects
BIOSYNTHESIS, MONOCYTES, SIRTUINS, DEACETYLASES, CHITIN deacetylase
Abstract

Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step in the salvage pathway for nicotinamide adenine dinucleotide (NAD+) biosynthesis, and thereby regulates the deacetylase activity of sirtuins. Here we show accommodative regulation of myocardial NAD+ by monocyte-derived extracellular Nampt (eNampt), which is essential for hemodynamic compensation to pressure overload. Although intracellular Nampt (iNampt) expression was decreased in pressure-overloaded hearts, myocardial NAD+ concentration and Sirt1 activity were preserved. In contrast, iNampt was up-regulated in spleen and monocytes, and circulating eNampt protein and nicotinamide mononucleotide (NMN), a key precursor of NAD+, were significantly increased. Pharmacological inhibition of Nampt by FK866 or depletion of monocytes/macrophages by clodronate liposomes disrupted the homeostatic mechanism of myocardial NAD+ levels and NAD+-dependent Sirt1 activity, leading to susceptibility to cardiomyocyte apoptosis and cardiac decompensation in pressure-overloaded mice. These biochemical and hemodynamic defects were prevented by systemic administration of NMN. Our studies uncover a crucial role of monocyte-derived eNampt in myocardial adaptation to pressure overload, and highlight a potential intervention controlling myocardial NAD+ against heart failure. [ABSTRACT FROM AUTHOR]

Published
2015
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