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Negative-feedback regulation of ATP release : ATP release from cardiomyocytes is strictly regulated during ischemia

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/48229

Title: Negative-feedback regulation of ATP release : ATP release from cardiomyocytes is strictly regulated during ischemia
Authors: Kunugi, Satohiko Browse this author
Iwabuchi, Sadahiro Browse this author
Matsuyama, Daisuke Browse this author
Okajima, Takaharu Browse this author →KAKEN DB
Kawahara, Koichi Browse this author →KAKEN DB
Keywords: ATP release
Cardiomyocytes
Maxi-anion channel
Hemichannel
Purinoceptor
Issue Date: 16-Dec-2011
Publisher: Elsevier
Journal Title: Biochemical and Biophysical Research Communications
Volume: 416
Issue: 3-4
Start Page: 409
End Page: 415
Publisher DOI: 10.1016/j.bbrc.2011.11.068
PMID: 22133679
Abstract: Extracellular ATP acts as a potent agonist on cardiomyocytes, inducing a broad range of physiological responses via P2 purinoceptors. Its concentration in the interstitial space within the heart is elevated during ischemia or hypoxia due to its release from a number of cell types, including cardiomyocytes. However, the exact mechanism responsible for the release of ATP from cardiomyocytes during ischemia is not known. In this study, we investigated whether and how the release of ATP was strictly regulated during ischemia in cultured neonatal rat cardiomyocytes. lschemia was mimicked by oxygen-glucose deprivation (OGD). Exposure of cardiomyocytes to OGD resulted in an increase in the concentration of extracellular ATP shortly after the onset of OGD (15 min), and the increase was reversed by treatment with blockers of maxi-anion channels. Unexpectedly, at 1 and 2 hours after the onset of OGD, the blocking of maxi-anion channels increased the concentration of extracellular ATP, and the increase was significantly suppressed by co-treatment with blockers of hemichannels, suggesting that ATP release via maxi-anion channels was involved in the suppression of ATP release via hemichannels during persistent OGD. Here we show the possibility that the release of ATP from cardiomyocytes was strictly regulated during ischemia by negative-feedback mechanisms; that is, maxi-anion channel-derived ATP-induced suppression of ATP release via hemichannels in cardiomyocytes.
Type: article (author version)
URI: http://hdl.handle.net/2115/48229
Appears in Collections:情報科学院・情報科学研究院 (Graduate School of Information Science and Technology / Faculty of Information Science and Technology) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 河原 剛一

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