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Cited by 31Mitochondrial Function and PathologyCancer, Hypoxia, and MetabolismCell death mechanisms and regulation

Proteome and cytoskeleton responses in osteosarcoma cells with reduced OXPHOS activity

Annunen‐Rasila, Johanna, Ohlmeier, Steffen, Tuokko, Hanna, Veijola, Johanna, Majamaa, Kari·2007·PROTEOMICS
DOI 10.1002/pmic.200601031
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Abstract

We have recently shown disorganization of the vimentin network in cultured cells deficient in oxidative phosphorylation (OXPHOS). We describe here the cellular responses to OXPHOS deficiency in osteosarcoma cells upon complex I (CI) and complex IV (CIV) inhibition, and upon the lack of mitochondrial DNA (rho0 cells). We examined the cytoskeletal organization and the distribution of mitochondria and analysed total proteome by 2-DE and vimentin expression by ELISA. Upon CIV inhibition and in rho0 cells, the vimentin network had collapsed around the nucleus and formed thick bundles. The mitochondria formed a perinuclear crescent upon CIV inhibition, whereas they accumulated around the nucleus in the rho0 cells, where the amount of vimentin was increased. Analysis of the total proteome revealed that a lack of mitochondrial DNA or inhibition of CI or CIV led to changes in the expression of cytoskeletal and cytoskeleton-associated proteins and proteins involved in apoptosis, OXPHOS, glycolysis, the tricarboxylic acid cycle, and oxidative stress responses. Our findings suggest that a deficiency in the energy converting system and oxidative stress can lead to cytoskeletal changes.

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Crossref · 10.1002/pmic.200601031

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  • Inhibition of CI or CIV caused changes in expression levels of apoptotic, cytoskeletal, and OXPHOS proteins, as well as proteins involved in TCA cycle, glycolysis, and oxidative stress responses.

    “Inhibition of CI or CIV caused changes in the expression levels of apoptotic, cytoskeletal, and OXPHOS proteins, as well as proteins involved in TCA cycle, glycolysis, and oxidative stress responses.”

    From Mitochondrial DNA mutations and human disease (2010) · cites this paper as [224]

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Authors
Annunen‐Rasila, J., Ohlmeier, S., Tuokko, H., Veijola, J., & Majamaa, K.
Affiliations
  • Oulu University Hospital (FI)
  • University of Oulu (FI)
  • University of Turku (FI)
Corresponding author
Majamaa, Kari
ORCID
Venue
PROTEOMICS
Publisher
Wiley
Published
2007-06
Volume
7
Issue
13
Pages
2189-2200
ISSN
  • 1615-9853 (ISSN-L)
  • 1615-9861
DOI
10.1002/pmic.200601031
OpenAlex
W2039613960
Cited by
31
References
60
Citations by year
2026: 1 · 2022: 1 · 2021: 1 · 2019: 2 · 2016: 3 · 2014: 3 · 2013: 3 · 2012: 2
FWCI
1.71
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • PROTEOMICS (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
osteosarcoma, oxidative phosphorylation deficiency, vimentin, cytoskeleton, mitochondrial DNA deletions, mitochondrial complex I inhibition, complex IV inhibition, mitochondrial distribution, proteome, oxidative stress, apoptosis, glycolysis, TCA cycle
MeSH terms
Electron Transport Complex IV, Cytoskeletal Proteins, Cytoskeleton, DNA, Mitochondrial, Energy Metabolism, Humans, Mitochondria, Mutation, Oxidative Phosphorylation, Proteins, Rotenone, Osteosarcoma, Vimentin, Electrophoresis, Gel, Two-Dimensional, Down-Regulation, Up-Regulation, Oxidative Stress, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, Sodium Azide, Proteome, Mitochondrial Proteins, Electron Transport Complex I, Cell Line, Tumor, Apoptosis Regulatory Proteins

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