Knockdown of apoptosis-inducing factor disrupts function of respiratory complex I
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
23682427
Knihovny.cz E-zdroje
- MeSH
- buněčné linie MeSH
- faktor vyvolávající apoptózu genetika fyziologie MeSH
- fenantridiny farmakologie MeSH
- fluorescenční barviva farmakologie MeSH
- HeLa buňky MeSH
- lidé MeSH
- mitochondriální membrány metabolismus MeSH
- mitochondrie metabolismus MeSH
- nádorové buněčné linie MeSH
- počítačové zpracování obrazu MeSH
- respirační komplex I metabolismus MeSH
- superoxidy metabolismus MeSH
- telomerasa metabolismus MeSH
- telomery ultrastruktura MeSH
- umlčování genů MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 5-(6'-triphenylphosphoniumhexyl)-5,6-dihydro-6-phenyl-3,8-phenanthridinediammine MeSH Prohlížeč
- faktor vyvolávající apoptózu MeSH
- fenantridiny MeSH
- fluorescenční barviva MeSH
- respirační komplex I MeSH
- superoxidy MeSH
- telomerasa MeSH
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.