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Mol. Cells 2003; 15(2): 256-261

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

Blockade of Calcium Entry Accelerates Arsenite-mediated Apoptosis in Rat Cerebellar Granule Cells

Uk Namgung, Dong-Hee Kim, Seok-Rhin Lim, Zhengui Xia

Abstract

Arsenical exposure can cause defects in the central nervous system, yet the underlying cellular and mo-lecular mechanisms are largely unknown. We have recently demonstrated that sodium arsenite induces apoptosis of cultured cortical and cerebellar neurons, suggesting that arsenite-induced neuronal apoptosis may contribute to at least some of its neurotoxic ef-fects. Here we investigated the effect of Ca2+ on ar-senite-mediated cerebellar granule neuron death. So-dium arsenite induced apoptosis in cerebellar neurons which were maintained in the presence of serum and depolarizing concentrations of potassium chloride (25 mM KCl). Under these conditions, inhibition of cal-cium entry by N-methyl-D-aspartate (NMDA) receptor blocker DL-aminophosphonovalerate (APV) or cal-cium channel antagonist nifedipine increased arsenite-induced apoptosis, while APV or nifedipine alone had little effect on cell viability. In cortical neurons or cerebellar neurons maintained at low potassium (5 mM), arsenite also induced apoptosis. However, the addition of APV or nifedipine did not alter levels of arsenite-induced apoptosis. These data suggest that arsenite-mediated apoptosis is regulated by intracellu-lar calcium levels.

Keywords Cerebellar Neurons, NMDA Receptor, Calcium Channel, Sodium Arsenite, Apoptosis, Calcium

Article

Research Article

Mol. Cells 2003; 15(2): 256-261

Published online April 30, 2003

Copyright © The Korean Society for Molecular and Cellular Biology.

Blockade of Calcium Entry Accelerates Arsenite-mediated Apoptosis in Rat Cerebellar Granule Cells

Uk Namgung, Dong-Hee Kim, Seok-Rhin Lim, Zhengui Xia

Abstract

Arsenical exposure can cause defects in the central nervous system, yet the underlying cellular and mo-lecular mechanisms are largely unknown. We have recently demonstrated that sodium arsenite induces apoptosis of cultured cortical and cerebellar neurons, suggesting that arsenite-induced neuronal apoptosis may contribute to at least some of its neurotoxic ef-fects. Here we investigated the effect of Ca2+ on ar-senite-mediated cerebellar granule neuron death. So-dium arsenite induced apoptosis in cerebellar neurons which were maintained in the presence of serum and depolarizing concentrations of potassium chloride (25 mM KCl). Under these conditions, inhibition of cal-cium entry by N-methyl-D-aspartate (NMDA) receptor blocker DL-aminophosphonovalerate (APV) or cal-cium channel antagonist nifedipine increased arsenite-induced apoptosis, while APV or nifedipine alone had little effect on cell viability. In cortical neurons or cerebellar neurons maintained at low potassium (5 mM), arsenite also induced apoptosis. However, the addition of APV or nifedipine did not alter levels of arsenite-induced apoptosis. These data suggest that arsenite-mediated apoptosis is regulated by intracellu-lar calcium levels.

Keywords: Cerebellar Neurons, NMDA Receptor, Calcium Channel, Sodium Arsenite, Apoptosis, Calcium

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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