Moisoi 2017 MiP2017

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Nicoleta Moisoi
Mitochondria-nucleus communication. Linking Parkinson’s related mitochondrial dysfunction with DNA damage signaling.

Link: MiP2017

Temelie M, Savu DI, Moisoi N (2017)

Event: MiP2017

COST Action MITOEAGLE

With a population growing in age, the prevalence of Parkinson’s disease (PD) as an age-related neurodegenerative disorder is rising. Dysfunction in mitochondrial quality control has been recognized as one of the main ethiopathological factors in PD. In addition, PD neurodegeneration is critically influenced by aging, process associated with accumulation of DNA damage. Cellular response to DNA lesions comprises a series of interconnected complex protective pathways. These are involved in intracellular as well as extracellular signaling of damage. Here we have initiated a study that addresses how the mitochondrial nucleus communication may occur in PD and what are the consequences of this interaction on the cell system.

In this work, we used cells deficient for PINK1, a mitochondrial kinase involved in mitochondria quality control whose loss-of-function leads to early onset PD challenged with inducers of DNA damage. Our studies revealed exacerbated sensibility to genotoxic stress in PINK1 deficient cells. We have also analysed changes that are induced by DNA damage in specific signalling pathways related to compartmental stress responses (including mitochondrial endoplasmic reticulum and cytoplasmic stress), DNA damage and repair signalling, as well as oxydative stress responses. The data demonstrates that PINK1 modulates these signalling pathways showing cell-type dependent characteristics.


Bioblast editor: Kandolf G O2k-Network Lab: UK Leicester Moisoi N


Labels: MiParea: nDNA;cell genetics, mt-Medicine  Pathology: Aging;senescence, Parkinson's 







Affiliations

Temelie M(1), Savu DI(1), Moisoi N(2)
  1. Nat Inst Physics Nuclear Engineering, Bucharest, Romania
  2. De Montfort Univ, Leicester, United Kingdom