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Influence of a mitochondrial genetic defect on capacitative calcium entry and mitochondrial organization in the osteosarcoma cells
Authors:Szczepanowska Joanna  Zabłocki Krzysztof  Duszyński Jerzy
Affiliation:Department of Cellular Biochemistry, Nencki Institute of Experimental Biology, Pasteura 3, 02 093 Warsaw, Poland. j.szczepanowska@nencki.gov.pl
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.
Keywords:[Ca2+]c, cytosolic calcium concentration   CCCP, carbonyl cyanide m-chlorophenyl hydrazone   CCE, capacitative calcium entry   DMSO, dimethyl sulfoxide   ER, endoplasmic reticulum   JC-1, 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazole carbocyanide iodide   mtDNA, mitochondrial DNA   MTs, microtubules   NARP, neurogenic muscle weakness, ataxia and retinitis pigmentosa   ΔΨ, mitochondrial membrane electric potential   PM, plasma membrane
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