TITLE

Differential gene expression during apoptosis induced by a serum factor: Role of mitochondrial F0-F1 ATP synthase complex

AUTHOR(S)
Singh, S.; Khar, A.
PUB. DATE
November 2005
SOURCE
Apoptosis;Nov2005, Vol. 10 Issue 6, p1469
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
The number of genes that are up regulated or down regulated during apoptosis is large and still increasing. In an attempt to characterize differential gene expression during serum factor induced apoptosis in AK-5 cells (a rat histiocytoma), we found subunit 6 and subunit 8 of the transmembrane proton channel and subunit alpha of the catalytic core of the mitochondrial F0-F1 ATP synthase complex to be up regulated during apoptosis. The increase in the expression levels of these subunits was concomitant with a transient increase in the intracellular ATP levels, suggesting that the increase in cellular ATP content is a result of the increase in the expression of ATP synthase subunits' gene and de novo protein synthesis. Depleting the cellular ATP levels with oligomycin inhibited apoptosis significantly, pointing to the requirement of ATP during apoptosis. Caspase 1 and caspase 3 activity and the loss of mitochondrial membrane potential were also inhibited by oligomycin during apoptosis in these cells, suggesting that the oligomycin induced inhibition of apoptosis could be due to inhibition of caspase activity and inhibition of mitochondrial depolarization. However, cytochrome C release during apoptosis was found to be completely independent of intracellular ATP content. Besides the ATP synthase complex genes, other mitochondrial genes like cytochrome C oxidase subunit II and III also showed elevated levels of expression during apoptosis. This kind of a mitochondrial gene expression profile suggests that in AK-5 cells, these genes are upregulated in a time-linked manner to ensure sufficient intracellular ATP levels and an efficient functioning of the mitochondrial respiratory chain for successful completion of the apoptotic pathway.
ACCESSION #
19474059

 

Related Articles

  • Bax targeting to mitochondria occurs via both tail anchor-dependent and -independent mechanisms. Valentijn, A. J.; Upton, J.-P.; Bates, N.; Gilmore, A. P. // Cell Death & Differentiation;Aug2008, Vol. 15 Issue 8, p1243 

    Bax is a member of the Bcl-2 family that, together with Bak, is required for permeabilisation of the outer mitochondrial membrane (OMM). Bax differs from Bak in that it is predominantly cytosolic in healthy cells and only associates with the OMM after an apoptotic signal. How Bax is targeted to...

  • OPINION: Breaking the mitochondrial barrier. Martinou, Jean-Claude; Green, Douglas R. // Nature Reviews Molecular Cell Biology;Jan2001, Vol. 2 Issue 1, p63 

    Pro- and anti-apoptotic members of the Bcl-2 family control the permeability of the outer mitochondrial membrane. They could do this either by forming autonomous pores in the membrane or by collaborating with components of the permeability transition pore. Here we discuss why we favour the first...

  • Association of fission proteins with mitochondrial raft-like domains. Ciarlo, L.; Manganelli, V.; Garofalo, T.; Matarrese, P.; Tinari, A.; Misasi, R.; Malorni, W.; Sorice, M. // Cell Death & Differentiation;Jun2010, Vol. 17 Issue 6, p1047 

    It was shown that receptor-mediated apoptosis involves a cascade of subcellular events including alterations of mitochondria. Loss of mitochondrial membrane potential that follows death receptor ligation allows the release of apoptogenic factors that result in apoptosis execution. Further...

  • The permeability transition and BCL-2 family proteins in apoptosis: co-conspirators or independent agents? Forte, M.; Bernardi, P. // Cell Death & Differentiation;Aug2006, Vol. 13 Issue 8, p1287 

    The article discusses on the permeability transition and Bcl-2 family proteins in the programmed death of cells. The apoptopic process in most vertebrates involves the permeabilization of the outer mitochodrial membrane resulting in the release of a variety of proteins activating between the...

  • Upstream control of apoptosis by caspase-2 in serum-deprived primary neurons. Chauvier, D.; Lecoeur, H.; Langonn&a#x00E9;, A.; Borgne-Sanchez, A.; Mariani, J.; Martinou, J.-C.; Rebouillat, D.; Jacotot, E. // Apoptosis;Nov2005, Vol. 10 Issue 6, p1243 

    During development as well as in pathological situations, neurons that fail to find appropriate targets or neurotrophic factors undergo cell death. Using primary cortical neurons subjected to acute serum-deprivation (SD), we have examined caspases activation, mitochondrial dysfunction and cell...

  • The Protective Effect of Stichopus Japonicus Fucoidan on PC12 Cells With Hypoxia/Reoxygenation Injury. Shuliang Song; Wei Wang; Xiaochen Wang; Hao Liang; Yunshan Wang; Aiguo Ji // Applied Mechanics & Materials;2014, Issue 556-562, p610 

    In this study the effect of fucoidan SJP-3 extracted from Stichopus Japonicus was used to evaluate the protective effect on PC12 cells with hypoxia/reoxygenation injury. SJP-3 can stabilize the mitochondrial membrane potential and resistant Cyt-C/mitochondrial apoptotic pathway via increasing...

  • Caspase-3 activation is an early event and initiates apoptotic damage in a human leukemia cell line. Varghese, J.; Khandre, N. S.; Sarin, A. // Apoptosis;Aug2003, Vol. 8 Issue 4, p363 

    Many apoptotic pathways culminate in the activation of caspase cascades usually triggered by the apical caspases-8 or -9. We describe a paradigm where apoptosis is initiated by the effector caspase-3. Diethylmaleate (DEM)-induced apoptotic damage in Jurkat cells was blocked by the anti-apoptotic...

  • Dynamical Systems Analysis of Mitochondrial BAK Activation Kinetics Predicts Resistance to BH3 Domains. Grills, Claire; Crawford, Nyree; Chacko, Alex; Johnston, Patrick G.; O'Rourke, Francesca; Fennell, Dean A. // PLoS ONE;2008, Vol. 3 Issue 8, p1 

    Introduction: The molecular mechanism underlying mitochondrial BAK activation during apoptosis remains highly controversial. Two seemingly conflicting models have been proposed. In one, BAK requires so-called activating BH3 only proteins (aBH3) to initiate its conformation change. In the other,...

  • Impact of Methylglyoxal and High Glucose Co-treatment on Human Mononuclear Cells. Ming-Shu Hsieh; Wen-Hsiung Chan // International Journal of Molecular Sciences;Apr2009, Vol. 10 Issue 4, p1445 

    Hyperglycemia and elevation of methylglyoxal (MG) are symptoms of diabetes mellitus (DM). In this report, we show that co-treatment of human mononuclear cells (HMNCs) with MG (5 μM) and high glucose (HG; 15 - 30 mM) induces apoptosis or necrosis. HG/MG co-treatment directly enhanced the...

Share

Read the Article

Courtesy of THE LIBRARY OF VIRGINIA

Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics