Difference between revisions of "Wojtala 2014 Abstract MiP2014"
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{{Abstract | {{Abstract | ||
|title= | |title=Proteomic analysis of mitochondrial Complex I deficient mouse model - impact of Complex I deficiency on p66Shc-Ser36 phosphorylation pathway in NDUFS4<sup>-/-</sup> mouse tissues. | ||
|info=[[File: | |info=[[File:Wojtala_A.jpg|150px|right|Wojtala A]] [[Laner 2014 Mitochondr Physiol Network MiP2014|Mitochondr Physiol Network 19.13]] - [http://www.mitophysiology.org/index.php?mip2014 MiP2014] | ||
|authors= | |authors=Wojtala A, Koopman Werner JH, Willems PH, Smeitink JA, Duszynski J, Wieckowski MR | ||
|year=2014 | |year=2014 | ||
|event=MiP2014 | |event=MiP2014 | ||
|abstract= | |abstract=Key mitochondrial energy-providing reactions are carried out by the oxidative phosphorylation system (OXPHOS), involving the electron transfer and phosphorylation systems including F<sub>1</sub>F<sub>o</sub>-ATP synthase. The most common OXPHOS disorder in humans is associated with Complex I deficiency, leading to fatal encephalomyopathies of early childhood- Leigh-like syndrome [1]. The growth factor adaptor protein p66Shc has a substantial impact on mitochondrial metabolism through regulation of cellular responses to oxidative stress. A low level of p66Shc protein or its complete ablation protects against numerous age-related disorders and may partially prevent pathologies caused by reactive oxygen species (ROS). On the other hand, a high level of p66Shc phosphorylation is correlated with increased intracellular ROS production [2,3]. | ||
Organs from NDUFS4<sup>-/-</sup> mice with Complex I deficiency were used as a model of self-propelling intracellular oxidative stress. The status of the antioxidant defense system, oxidative stress markers and the p66Shc-Ser36 phosphorylation pathway were measured in these tissues. Mass spectrometry analysis was also performed for selected NDUFS4<sup>-/-</sup> mouse tissues. | |||
In our study, mice with defective Complex I were characterized by attenuated intracellular oxidative stress, connected with increased p66Shc phosphorylation. Mass spectrometry revealed aberrations in the level of Complex I proteins and oxidative stress- related proteins, as well as other proteins involved in metabolic processes. | |||
|mipnetlab=NL Nijmegen Koopman WJ | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|injuries=Oxidative stress;RONS | |||
|organism=Mouse | |||
|enzymes=Complex I | |||
|event=A1, P-flash | |||
|additional=MiP2014 | |additional=MiP2014 | ||
}} | }} | ||
== Affiliation == | == Affiliation == | ||
1-Dep Biochem, Nencki Inst Experimental Biol, Warsaw, Poland; 2-Radbound Univ Medical Centre, Nijmegen, The Netherlands. - a.wojtala@nencki.gov.pl | |||
== References and acknowledgements == | |||
This work was supported by the Statutory Founding from Nencki Institute of Experimental Biology and Polish Ministry of Science and Higher Education grant W100/HFSC/2011. | |||
# Distelmaier F, Koopmann WJ, van den Heuvel PL, Rodenburg RJ, Mayatepek E, Willems PH, Smeitink JA (2009) Mitochondrial complex I deficiency: from organelle dysfunction to clinical disease. Brain 132: 833–42. | |||
# Pinton P, Rimessi A, Marchi S, Orsini F, Migliaccio E, Giorgio M, Contursi C, Minucci S, Mantovani F, Wieckowski MR, Del Sal G, Pelicci PG, Rizzuto R (2007) Protein kinase C beta and prolyl isomerase 1 regulate mitochondrial effects of the life-span determinant p66Shc. Science 315: 659-63. | |||
# Suski JM, Karkucinska-Wieckowska A, Lebiedzinska M, Giorgi C, Szczepanowska J, Szabadkai G, Duszynski J, Pronicki M, Pinton P, Wieckowski MR (2011) p66Shc aging protein in control of fibroblasts cell fate. Int J Mol Sci 12: 5373-89. | |||
Latest revision as of 09:00, 18 March 2020
| Proteomic analysis of mitochondrial Complex I deficient mouse model - impact of Complex I deficiency on p66Shc-Ser36 phosphorylation pathway in NDUFS4-/- mouse tissues. |
Link:
Mitochondr Physiol Network 19.13 - MiP2014
Wojtala A, Koopman Werner JH, Willems PH, Smeitink JA, Duszynski J, Wieckowski MR (2014)
Event: MiP2014
Key mitochondrial energy-providing reactions are carried out by the oxidative phosphorylation system (OXPHOS), involving the electron transfer and phosphorylation systems including F1Fo-ATP synthase. The most common OXPHOS disorder in humans is associated with Complex I deficiency, leading to fatal encephalomyopathies of early childhood- Leigh-like syndrome [1]. The growth factor adaptor protein p66Shc has a substantial impact on mitochondrial metabolism through regulation of cellular responses to oxidative stress. A low level of p66Shc protein or its complete ablation protects against numerous age-related disorders and may partially prevent pathologies caused by reactive oxygen species (ROS). On the other hand, a high level of p66Shc phosphorylation is correlated with increased intracellular ROS production [2,3].
Organs from NDUFS4-/- mice with Complex I deficiency were used as a model of self-propelling intracellular oxidative stress. The status of the antioxidant defense system, oxidative stress markers and the p66Shc-Ser36 phosphorylation pathway were measured in these tissues. Mass spectrometry analysis was also performed for selected NDUFS4-/- mouse tissues.
In our study, mice with defective Complex I were characterized by attenuated intracellular oxidative stress, connected with increased p66Shc phosphorylation. Mass spectrometry revealed aberrations in the level of Complex I proteins and oxidative stress- related proteins, as well as other proteins involved in metabolic processes.
• O2k-Network Lab: NL Nijmegen Koopman WJ
Labels:
Stress:Oxidative stress;RONS Organism: Mouse
Enzyme: Complex I
Event: A1, P-flash
MiP2014
Affiliation
1-Dep Biochem, Nencki Inst Experimental Biol, Warsaw, Poland; 2-Radbound Univ Medical Centre, Nijmegen, The Netherlands. - a.wojtala@nencki.gov.pl
References and acknowledgements
This work was supported by the Statutory Founding from Nencki Institute of Experimental Biology and Polish Ministry of Science and Higher Education grant W100/HFSC/2011.
- Distelmaier F, Koopmann WJ, van den Heuvel PL, Rodenburg RJ, Mayatepek E, Willems PH, Smeitink JA (2009) Mitochondrial complex I deficiency: from organelle dysfunction to clinical disease. Brain 132: 833–42.
- Pinton P, Rimessi A, Marchi S, Orsini F, Migliaccio E, Giorgio M, Contursi C, Minucci S, Mantovani F, Wieckowski MR, Del Sal G, Pelicci PG, Rizzuto R (2007) Protein kinase C beta and prolyl isomerase 1 regulate mitochondrial effects of the life-span determinant p66Shc. Science 315: 659-63.
- Suski JM, Karkucinska-Wieckowska A, Lebiedzinska M, Giorgi C, Szczepanowska J, Szabadkai G, Duszynski J, Pronicki M, Pinton P, Wieckowski MR (2011) p66Shc aging protein in control of fibroblasts cell fate. Int J Mol Sci 12: 5373-89.
