Aluminium Inhibits Muscarinic Agonist-Induced Inositol 1,4,5-Trisphosphate Production and Calcium Mobilization in Permeabilized SH-SY5Y Human Neuroblastoma Cells
| Autor: | Stefan R. Nahorski, J. Burgess, P. C. Wood, Richard J.H. Wojcikiewicz, C. M. Castleden |
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| Rok vydání: | 2008 |
| Předmět: |
medicine.medical_specialty
SH-SY5Y chemistry.chemical_element Inositol 1 4 5-Trisphosphate Calcium Biochemistry Muscarinic agonist Permeability Neuroblastoma Cellular and Molecular Neuroscience chemistry.chemical_compound Internal medicine Muscarinic acetylcholine receptor Tumor Cells Cultured medicine Humans Inositol Phosphatidylinositol Inositol phosphate chemistry.chemical_classification integumentary system Inositol trisphosphate Endocrinology Parasympathomimetics chemistry Biophysics Aluminum |
| Zdroj: | Journal of Neurochemistry. 62:2219-2223 |
| ISSN: | 1471-4159 0022-3042 |
| DOI: | 10.1046/j.1471-4159.1994.62062219.x |
| Popis: | The effects of aluminium (as Al3+) on carbachol-induced inositol 1,4,5-trisphosphate (InsP3) production and Ca2+ mobilisation were assessed in electropermeabilised human SH-SY5Y neuroblastoma cells. Al3+ had no effect on InsP3-induced Ca2+ release but appreciably reduced carbachol-induced Ca2+ release (IC50 of approximately 90 microM). Al3+ also inhibited InsP3 production (IC50 of approximately 15 microM). Dimethyl hydroxypyridin-4-one, a potent Al3+ chelator (Ks = 31), at 100 microM was able to abort and reverse the effects of Al3+ on both Ca2+ release and InsP3 production. These data suggest that, in permeabilised cells, the effect of Al3+ on the phosphoinositide-mediated signalling pathway is at the level of phosphatidylinositol 4,5-bisphosphate hydrolysis. This may reflect interference with receptor-G protein-phospholipase C coupling or an interaction with phosphatidylinositol 4,5-bisphosphate. |
| Databáze: | OpenAIRE |
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