Difference between revisions of "Rubelj 2018 MiP2018"
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{{Abstract | {{Abstract | ||
|title=[[Image: | |title=[[Image:File:RubeljI.JPG|left|90px|Ivica Rubelj]] Role of mitochondria in mammalian senescence and aging. | ||
|info=[[MiP2018]] | |info=[[MiP2018]] | ||
|authors=Nanic L, Rubelj I | |authors=Nanic L, Rubelj I | ||
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|event=MiP2018 | |event=MiP2018 | ||
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]] | |abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]] | ||
Fundamental property of somatic cells in higher mammals is their limited division capacity ending in cellular senescence. Two main mechanisms contribute to cellular senescence, telomere shortening and damaging effects of free radicals, mostly generated by mitochondria. It is well established that these two mechanisms are in mutual interactions but many aspects of these interactions still remain to be elucidated. This was clearly demonstrated in the experiments in which cell growth and senescence, as well as telomere shortening are directly dependent on oxygen partial pressure (1). However, expression of telomerase (TERT), an enzyme that extends telomeres, recovered cells from senescence and restored mitochondrial function. This includes TERT translocation from the nucleus and localisation to mitochondria. It appears that TERT protects mitochondria from hyperoxia-induced damage in a way that both mitochondrial DNA damage and superoxide production decrease and the mitochondrial membrane potential elevates. Also these cells have enhanced resistance to apoptosis | Fundamental property of somatic cells in higher mammals is their limited division capacity ending in cellular senescence. Two main mechanisms contribute to cellular senescence, telomere shortening and damaging effects of free radicals, mostly generated by mitochondria. It is well established that these two mechanisms are in mutual interactions but many aspects of these interactions still remain to be elucidated. This was clearly demonstrated in the experiments in which cell growth and senescence, as well as telomere shortening are directly dependent on oxygen partial pressure (1). However, expression of telomerase (TERT), an enzyme that extends telomeres, recovered cells from senescence and restored mitochondrial function. This includes TERT translocation from the nucleus and localisation to mitochondria. It appears that TERT protects mitochondria from hyperoxia-induced damage in a way that both mitochondrial DNA damage and superoxide production decrease and the mitochondrial membrane potential elevates. Also these cells have enhanced resistance to apoptosis [2]. This lecture will present newest findings in research on cell senescence, aging and rejuvenation and the role of mitochondria in these processes. | ||
|editor=[[Plangger M]], [[Kandolf G]], | |editor=[[Plangger M]], [[Kandolf G]], | ||
}} | }} | ||
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}} | }} | ||
== Affiliations == | == Affiliations == | ||
::::Lab Molecular Cellular Biology, Div Molecular Biology, Ruđer Bošković Inst, Zagreb, Croatia | ::::Lab Molecular Cellular Biology, Div Molecular Biology, Ruđer Bošković Inst, Zagreb, Croatia. - ivica.rubelj@irb.hr | ||
== References == | == References == | ||
::::#von Zglinicki T (2002) Oxidative stress shortens telomeres. Trends Biochem Sci 27:339-44. | ::::#von Zglinicki T (2002) Oxidative stress shortens telomeres. Trends Biochem Sci 27:339-44. | ||
::::#Ahmed S, Passos JF, Birket MJ, Beckmann T, Brings S, Peters H, Birch-Machin MA, von Zglinicki T, Saretzki G (2008) Telomerase does not counteract telomere shortening but protects mitochondrial function under oxidative stress. J Cell Sci 121:1046-53. | ::::#Ahmed S, Passos JF, Birket MJ, Beckmann T, Brings S, Peters H, Birch-Machin MA, von Zglinicki T, Saretzki G (2008) Telomerase does not counteract telomere shortening but protects mitochondrial function under oxidative stress. J Cell Sci 121:1046-53. | ||
Revision as of 16:43, 6 August 2018
| Role of mitochondria in mammalian senescence and aging. |
Link: MiP2018
Event: MiP2018
Fundamental property of somatic cells in higher mammals is their limited division capacity ending in cellular senescence. Two main mechanisms contribute to cellular senescence, telomere shortening and damaging effects of free radicals, mostly generated by mitochondria. It is well established that these two mechanisms are in mutual interactions but many aspects of these interactions still remain to be elucidated. This was clearly demonstrated in the experiments in which cell growth and senescence, as well as telomere shortening are directly dependent on oxygen partial pressure (1). However, expression of telomerase (TERT), an enzyme that extends telomeres, recovered cells from senescence and restored mitochondrial function. This includes TERT translocation from the nucleus and localisation to mitochondria. It appears that TERT protects mitochondria from hyperoxia-induced damage in a way that both mitochondrial DNA damage and superoxide production decrease and the mitochondrial membrane potential elevates. Also these cells have enhanced resistance to apoptosis [2]. This lecture will present newest findings in research on cell senescence, aging and rejuvenation and the role of mitochondria in these processes.
• Bioblast editor: Plangger M, Kandolf G
Labels: MiParea: mtDNA;mt-genetics Pathology: Aging;senescence
Affiliations
- Lab Molecular Cellular Biology, Div Molecular Biology, Ruđer Bošković Inst, Zagreb, Croatia. - ivica.rubelj@irb.hr
References
- von Zglinicki T (2002) Oxidative stress shortens telomeres. Trends Biochem Sci 27:339-44.
- Ahmed S, Passos JF, Birket MJ, Beckmann T, Brings S, Peters H, Birch-Machin MA, von Zglinicki T, Saretzki G (2008) Telomerase does not counteract telomere shortening but protects mitochondrial function under oxidative stress. J Cell Sci 121:1046-53.
