Open Access

ARTICLE

Knockdown of apoptosis-inducing factor disrupts function of respiratory complex

MIROSLAV VAŘECHA^1*, DANIELA PÁCLOVÁ², JIŘINA PROCHÁZKOVÁ², PAVEL MATULA¹, DUŠAN CMARKO³, AND MICHAL KOZUBEK¹

1. Centre for Biomedical Image Analysis, Faculty of Informatics, Masaryk University, Botanická 68a, Brno 60200, Czech Republic.
2. Department of Experimental Biology, Faculty of Science, Masaryk University, Kotlářská 2, Brno 61137, Czech Republic.
3. Institute of Cellular Biology and Pathology, 1st Faculty of Medicine, Charles University in Prague, Albertov 4, Prague 12801, Czech Republic.

*Address correspondence to: Miroslav Vařecha. Centre for Biomedical Image Analysis, Faculty of Informatics, Masaryk University, Botanická 68a, 60200 Brno, Czech Republic. Phone: +420 549 496 696, Fax: +420 549 494 023.

BIOCELL 2012, 36(3), 121-126. https://doi.org/10.32604/biocell.2012.36.121

Abstract

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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