Cellular calcium deficiency plays a role in neuronal death caused by proteasome inhibitors
| العنوان: | Cellular calcium deficiency plays a role in neuronal death caused by proteasome inhibitors |
|---|---|
| المؤلفون: | Krista L. Moulder, Krzysztof L. Hyrc, Shengzhou Wu, Timothy Warmke, B. Joy Snider, Ying Lin |
| المصدر: | Journal of Neurochemistry. 109:1225-1236 |
| بيانات النشر: | Wiley, 2009. |
| سنة النشر: | 2009 |
| مصطلحات موضوعية: | medicine.medical_specialty, Programmed cell death, Patch-Clamp Techniques, Time Factors, Leupeptins, Biophysics, Neocortex, Cysteine Proteinase Inhibitors, Endoplasmic Reticulum, Biochemistry, Article, Membrane Potentials, Amiloride, Lactones, Mice, Cellular and Molecular Neuroscience, Cytosol, Calcium imaging, Internal medicine, Excitatory Amino Acid Agonists, medicine, Animals, Uniporter, Cells, Cultured, Caspase, Neurons, Membrane potential, Cell Death, Dose-Response Relationship, Drug, biology, Endoplasmic reticulum, 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester, Calcium Channel Blockers, Embryo, Mammalian, Electric Stimulation, Cell biology, Endocrinology, Cell Death Process, Astrocytes, biology.protein, Calcium, Proteasome Inhibitors, Sesquiterpenes |
| الوصف: | Cytosolic Ca(2+) concentration ([Ca(2+)](i)) is reduced in cultured neurons undergoing neuronal death caused by inhibitors of the ubiquitin proteasome system. Activation of calcium entry via voltage-gated Ca(2+) channels restores cytosolic Ca(2+) levels and reduces this neuronal death (Snider et al. 2002). We now show that this reduction in [Ca(2+)](i) is transient and occurs early in the cell death process, before activation of caspase 3. Agents that increase Ca(2+) influx such as activation of voltage-gated Ca(2+) channels or stimulation of Ca(2+) entry via the plasma membrane Na-Ca exchanger attenuate neuronal death only if applied early in the cell death process. Cultures treated with proteasome inhibitors had reduced current density for voltage-gated Ca(2+) channels and a less robust increase in [Ca(2+)](i) after depolarization. Levels of endoplasmic reticulum Ca(2+) were reduced and capacitative Ca(2+) entry was impaired early in the cell death process. Mitochondrial Ca(2+) was slightly increased. Preventing the transfer of Ca(2+) from mitochondria to cytosol increased neuronal vulnerability to this death while blockade of mitochondrial Ca(2+) uptake via the uniporter had no effect. Programmed cell death induced by proteasome inhibition may be caused in part by an early reduction in cytosolic and endoplasmic reticulum Ca(2+,) possibly mediated by dysfunction of voltage-gated Ca(2+) channels. These findings may have implications for the treatment of disorders associated with protein misfolding in which proteasome impairment and programmed cell death may occur. |
| تدمد: | 1471-4159 0022-3042 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::47be7d5445536748fc2f989bdfeb66f6Test https://doi.org/10.1111/j.1471-4159.2009.06037.xTest |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....47be7d5445536748fc2f989bdfeb66f6 |
| قاعدة البيانات: | OpenAIRE |
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Activation of calcium entry via voltage-gated Ca(2+) channels restores cytosolic Ca(2+) levels and reduces this neuronal death (Snider et al. 2002). We now show that this reduction in [Ca(2+)](i) is transient and occurs early in the cell death process, before activation of caspase 3. Agents that increase Ca(2+) influx such as activation of voltage-gated Ca(2+) channels or stimulation of Ca(2+) entry via the plasma membrane Na-Ca exchanger attenuate neuronal death only if applied early in the cell death process. Cultures treated with proteasome inhibitors had reduced current density for voltage-gated Ca(2+) channels and a less robust increase in [Ca(2+)](i) after depolarization. Levels of endoplasmic reticulum Ca(2+) were reduced and capacitative Ca(2+) entry was impaired early in the cell death process. Mitochondrial Ca(2+) was slightly increased. Preventing the transfer of Ca(2+) from mitochondria to cytosol increased neuronal vulnerability to this death while blockade of mitochondrial Ca(2+) uptake via the uniporter had no effect. Programmed cell death induced by proteasome inhibition may be caused in part by an early reduction in cytosolic and endoplasmic reticulum Ca(2+,) possibly mediated by dysfunction of voltage-gated Ca(2+) channels. 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