Mitochondria are intracellular magnesium stores: Investigation by simultaneous fluorescent imagings in PC12 cells

Takeshi Kubota, Yutaka Shindo, Kentaro Tokuno, Hirokazu Komatsu, Hiroto Ogawa, Susumu Kudo, Yoshiichiro Kitamura, Koji Suzuki, Kotaro Oka

研究成果: ジャーナルへの寄稿記事

74 引用 (Scopus)

抄録

To determine the nature of intracellular Mg2+ stores and Mg 2+ release mechanisms in differentiated PC12 cells, Mg2+ and Ca2+ mobilizations were measured simultaneously in living cells with KMG-104, a fluorescent Mg2+ indicator, and fura-2, respectively. Treatment with the mitochondrial uncoupler, carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP), increased both the intracellular Mg2+ concentration ([Mg2+]i) and the [Ca 2+]i in these cells. Possible candidates as intracellular Mg2+ stores under these conditions include intracellular divalent cation binding sites, endoplasmic reticulum (ER), Mg-ATP and mitochondria. Given that no change in [Mg2+]i was induced by caffeine application, intracellular IP3 or Ca2+ liberated by photolysis, it appears that no Mg2+ release mechanism thus exists that is mediated via the action of Ca2+ on membrane-bound receptors in the ER or via the offloading of Mg2+ from binding sites as a result of the increased [Ca2+]i. FCCP treatment for 2 min did not alter the intracellular ATP content, indicating that Mg2+ was not released from Mg-ATP, at least in the first 2 min following exposure to FCCP. FCCP-induced [Mg2+]i increase was observed at mitochondria localized area, and vice versa. These results suggest that the mitochondria serve as the intracellular Mg2+ store in PC12 cell. Simultaneous measurements of [Ca2+]i and mitochondrial membrane potential, and also of [Ca2+]i and [Mg 2+]i, revealed that the initial rise in [Mg 2+]i followed that of mitochondrial depolarization for several seconds. These findings show that the source of Mg2+ in the FCCP-induced [Mg2+]i increase in PC12 cells is mitochondria, and that mitochondrial depolarization triggers the Mg2+ release.

元の言語英語
ページ(範囲)19-28
ページ数10
ジャーナルBiochimica et Biophysica Acta - Molecular Cell Research
1744
発行部数1
DOI
出版物ステータス出版済み - 5 15 2005
外部発表Yes

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Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
PC12 Cells
Magnesium
Mitochondria
Adenosine Triphosphate
Endoplasmic Reticulum
Binding Sites
Fura-2
Mitochondrial Membrane Potential
Photolysis
Divalent Cations
Caffeine
Membranes

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

これを引用

Mitochondria are intracellular magnesium stores : Investigation by simultaneous fluorescent imagings in PC12 cells. / Kubota, Takeshi; Shindo, Yutaka; Tokuno, Kentaro; Komatsu, Hirokazu; Ogawa, Hiroto; Kudo, Susumu; Kitamura, Yoshiichiro; Suzuki, Koji; Oka, Kotaro.

:: Biochimica et Biophysica Acta - Molecular Cell Research, 巻 1744, 番号 1, 15.05.2005, p. 19-28.

研究成果: ジャーナルへの寄稿記事

Kubota, Takeshi ; Shindo, Yutaka ; Tokuno, Kentaro ; Komatsu, Hirokazu ; Ogawa, Hiroto ; Kudo, Susumu ; Kitamura, Yoshiichiro ; Suzuki, Koji ; Oka, Kotaro. / Mitochondria are intracellular magnesium stores : Investigation by simultaneous fluorescent imagings in PC12 cells. :: Biochimica et Biophysica Acta - Molecular Cell Research. 2005 ; 巻 1744, 番号 1. pp. 19-28.
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abstract = "To determine the nature of intracellular Mg2+ stores and Mg 2+ release mechanisms in differentiated PC12 cells, Mg2+ and Ca2+ mobilizations were measured simultaneously in living cells with KMG-104, a fluorescent Mg2+ indicator, and fura-2, respectively. Treatment with the mitochondrial uncoupler, carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP), increased both the intracellular Mg2+ concentration ([Mg2+]i) and the [Ca 2+]i in these cells. Possible candidates as intracellular Mg2+ stores under these conditions include intracellular divalent cation binding sites, endoplasmic reticulum (ER), Mg-ATP and mitochondria. Given that no change in [Mg2+]i was induced by caffeine application, intracellular IP3 or Ca2+ liberated by photolysis, it appears that no Mg2+ release mechanism thus exists that is mediated via the action of Ca2+ on membrane-bound receptors in the ER or via the offloading of Mg2+ from binding sites as a result of the increased [Ca2+]i. FCCP treatment for 2 min did not alter the intracellular ATP content, indicating that Mg2+ was not released from Mg-ATP, at least in the first 2 min following exposure to FCCP. FCCP-induced [Mg2+]i increase was observed at mitochondria localized area, and vice versa. These results suggest that the mitochondria serve as the intracellular Mg2+ store in PC12 cell. Simultaneous measurements of [Ca2+]i and mitochondrial membrane potential, and also of [Ca2+]i and [Mg 2+]i, revealed that the initial rise in [Mg 2+]i followed that of mitochondrial depolarization for several seconds. These findings show that the source of Mg2+ in the FCCP-induced [Mg2+]i increase in PC12 cells is mitochondria, and that mitochondrial depolarization triggers the Mg2+ release.",
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AU - Kubota, Takeshi

AU - Shindo, Yutaka

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AU - Ogawa, Hiroto

AU - Kudo, Susumu

AU - Kitamura, Yoshiichiro

AU - Suzuki, Koji

AU - Oka, Kotaro

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