Influence of a mitochondrial genetic defect on capacitative calcium entry and mitochondrial organization in the osteosarcoma cells.

Jerzy Duszyński, Krzysztof Zabłocki, Joanna Szczepanowska

Journal: FEBS letters 2005;578(3):316-22

PMID: 15589839

Abstract

Effects of T8993G mutation in mitochondrial DNA (mtDNA), associated with neurogenical muscle weakness, ataxia and retinitis pigmentosa (NARP), on the cytoskeleton, mitochondrial network and calcium homeostasis in human osteosarcoma cells were investigated. In 98% NARP and rho(0) (lacking mtDNA) cells, the organization of the mitochondrial network and actin cytoskeleton was disturbed. Capacitative calcium entry (CCE) was practically independent of mitochondrial energy status in osteosarcoma cell lines. The significantly slower Ca(2+) influx rates observed in 98% NARP and rho(0), in comparison to parental cells, indicates that proper actin cytoskeletal organization is important for CCE in these cells.

Address: Department of Cellular Biochemistry, Nencki Institute of Experimental Biology, Pasteura 3, 02 093 Warsaw, Poland. [email protected]

DOI: 10.1016/j.febslet.2004.11.022

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MeSH Terms: Actins, Ataxia, Benzimidazoles, Calcium, Carbocyanines, Carbonyl Cyanide m-Chlorophenyl Hydrazone, Cell Line, Tumor, Cytoskeleton, DNA, Mitochondrial, Fluorescent Dyes, Fura-2, Humans, Image Processing, Computer-Assisted, Immunohistochemistry, Ionophores, Membrane Potentials, Microscopy, Fluorescence, Mitochondrial Myopathies, Muscle Weakness, Mutation, Osteosarcoma, Phalloidine, Retinitis Pigmentosa, Rhodamines, Thapsigargin