Knockdown of apoptosis-inducing factor disrupts function of respiratory complex I

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Název česky Snížení množství apoptózu vyvolávajícího faktoru narušuje funkci dýchacího komplexu I
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VAŘECHA Miroslav PÁCLOVÁ Daniela PROCHÁZKOVÁ Jiřina MATULA Pavel CMARKO Dušan KOZUBEK Michal

Rok publikování 2012
Druh Článek v odborném periodiku
Časopis / Zdroj BIOCELL
Fakulta / Pracoviště MU

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Citace
www http://www.scielo.org.ar/scielo.php?script=sci_issues&pid=0327-9545&lng=en&nrm=iso
Obor Genetika a molekulární biologie
Klíčová slova superoxide;fluorescence microscopy;image analysis;mitochondria;telomerase
Přiložené soubory
Popis Recent findings suggest that apoptotic protein apoptosis-inducing factor (AIF) may also play an important non-apoptotic function inside mitochondria. AIF was proposed to be an important component of respiratory chain complex I that is the major producer of superoxide radical. The possible role of AIF is still controversial. Superoxide production could be used as a valuable measure of complex I function, because the majority of superoxide is produced there. Therefore, we employed superoxide-specific mitochondrial fluorescence dye for detection of superoxide production. We studied an impact of AIF knockdown on function of mitochondrial complex I by analyzing superoxide production in selected cell lines. Our results show that tumoral telomerase-positive (TP) AIF knockdown cell lines display significant increase in superoxide production in comparison to control cells, while a non-tumoral cell line and tumoral telomerase-negative cell lines with alternative lengthening of telomeres (ALT) show a decrease in superoxide production. According to these results, we can conclude that AIF knockdown disrupts function of complex I and therefore increases the superoxide production in mitochondria. The distinct effect of AIF depletion in various cell lines could result from recently discovered activity of telomerase in mitochondria of TP cancer cells, but this hypothesis needs further investigation.
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