Abstract
Brain hypoxia or ischemia causes acidosis and the intracellular accumulation of Ca2+ in neuron. The aims of the present study were to elucidate the interaction between intracellular pH and Ca2+ during transient acidosis and its effects on the viability of neuronal and glial cells. Intracellular Ca2+ and pH were measured using the fluorescence of fura-2 and 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester in neuroblastoma (IMR-32), glioblastoma (T98G), and astrocytoma (CCF-STTG1) cell lines. The administration of 5 mM propionate caused intracellular acidification in IMR-32 and T98G cells but not in CCF-STTG1 cells. After the removal of propionate, the intracellular pH recovered to the resting level. The intracellular Ca2+ transiently increased upon the removal of propionate in IMR-32 and T98G cells but not in CCF-STTG1 cells. The transient Ca2+ increase caused by the withdrawal of intracellular acidification was abolished by the removal of external Ca2+, diminished by a reduction of external Na+, and inhibited by benzamil. Transient acidosis caused cell death, whereas the cells were more viable in the absence of external Ca2+. Benzamil alleviated cell death caused by transient acidosis in IMR-32 and T98G cells but not in CCF-STTG1 cells. These results suggest that recovery from intracellular acidosis causes a transient increase in cytosolic Ca2+ due to reversal of Ca2+ transport via Na+/Ca2+ exchanger coactivated with Na +/H+ exchanger, which can cause cell death.
| Original language | English |
|---|---|
| Pages (from-to) | 453-460 |
| Number of pages | 8 |
| Journal | Cellular and Molecular Neurobiology |
| Volume | 30 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Apr 1 2010 |
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All Science Journal Classification (ASJC) codes
- Cellular and Molecular Neuroscience
- Cell Biology
Cite this
Change in intracellular pH causes the toxic Ca2+ entry via NCX1 in neuron- and glia-derived cells. / shono, yuji; Kamouchi, Masahiro; Kitazono, Takanari; Kuroda, Junya; Nakamura, Kuniyuki; Hagiwara, Noriko; Ooboshi, Hiroaki; Ibayashi, Setsuro; Iida, Mitsuo.
In: Cellular and Molecular Neurobiology, Vol. 30, No. 3, 01.04.2010, p. 453-460.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Change in intracellular pH causes the toxic Ca2+ entry via NCX1 in neuron- and glia-derived cells
AU - shono, yuji
AU - Kamouchi, Masahiro
AU - Kitazono, Takanari
AU - Kuroda, Junya
AU - Nakamura, Kuniyuki
AU - Hagiwara, Noriko
AU - Ooboshi, Hiroaki
AU - Ibayashi, Setsuro
AU - Iida, Mitsuo
PY - 2010/4/1
Y1 - 2010/4/1
N2 - Brain hypoxia or ischemia causes acidosis and the intracellular accumulation of Ca2+ in neuron. The aims of the present study were to elucidate the interaction between intracellular pH and Ca2+ during transient acidosis and its effects on the viability of neuronal and glial cells. Intracellular Ca2+ and pH were measured using the fluorescence of fura-2 and 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester in neuroblastoma (IMR-32), glioblastoma (T98G), and astrocytoma (CCF-STTG1) cell lines. The administration of 5 mM propionate caused intracellular acidification in IMR-32 and T98G cells but not in CCF-STTG1 cells. After the removal of propionate, the intracellular pH recovered to the resting level. The intracellular Ca2+ transiently increased upon the removal of propionate in IMR-32 and T98G cells but not in CCF-STTG1 cells. The transient Ca2+ increase caused by the withdrawal of intracellular acidification was abolished by the removal of external Ca2+, diminished by a reduction of external Na+, and inhibited by benzamil. Transient acidosis caused cell death, whereas the cells were more viable in the absence of external Ca2+. Benzamil alleviated cell death caused by transient acidosis in IMR-32 and T98G cells but not in CCF-STTG1 cells. These results suggest that recovery from intracellular acidosis causes a transient increase in cytosolic Ca2+ due to reversal of Ca2+ transport via Na+/Ca2+ exchanger coactivated with Na +/H+ exchanger, which can cause cell death.
AB - Brain hypoxia or ischemia causes acidosis and the intracellular accumulation of Ca2+ in neuron. The aims of the present study were to elucidate the interaction between intracellular pH and Ca2+ during transient acidosis and its effects on the viability of neuronal and glial cells. Intracellular Ca2+ and pH were measured using the fluorescence of fura-2 and 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester in neuroblastoma (IMR-32), glioblastoma (T98G), and astrocytoma (CCF-STTG1) cell lines. The administration of 5 mM propionate caused intracellular acidification in IMR-32 and T98G cells but not in CCF-STTG1 cells. After the removal of propionate, the intracellular pH recovered to the resting level. The intracellular Ca2+ transiently increased upon the removal of propionate in IMR-32 and T98G cells but not in CCF-STTG1 cells. The transient Ca2+ increase caused by the withdrawal of intracellular acidification was abolished by the removal of external Ca2+, diminished by a reduction of external Na+, and inhibited by benzamil. Transient acidosis caused cell death, whereas the cells were more viable in the absence of external Ca2+. Benzamil alleviated cell death caused by transient acidosis in IMR-32 and T98G cells but not in CCF-STTG1 cells. These results suggest that recovery from intracellular acidosis causes a transient increase in cytosolic Ca2+ due to reversal of Ca2+ transport via Na+/Ca2+ exchanger coactivated with Na +/H+ exchanger, which can cause cell death.
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U2 - 10.1007/s10571-009-9470-7
DO - 10.1007/s10571-009-9470-7
M3 - Article
VL - 30
SP - 453
EP - 460
JO - Cellular and Molecular Neurobiology
JF - Cellular and Molecular Neurobiology
SN - 0272-4340
IS - 3
ER -