During Targeting Mitochondria 2011, the Scientific Committee awarded three researchers for their innovative projects


Dr Daniela Arduino, from Center for Neuroscience and Cell Biology, University of Coimbra, Portugal, was awarded for here scientific contribution for her work about SIRT2 DEACETYLASE ACTIVITY CONTROLS THE AUTOPHAGY-LYSOSOMAL SYSTEM BY MODULATING THE ACETYLATION DYNAMICS OF TUBULIN CYTOSKELETON.

More information about this work:

In Parkinson’s disease, mutational mtDNA signatures translate into mitochondrial dysfunction. We found that, under these conditions,
an impairment of microtubule- dependent trafficking ensues, perceived by excessive deacetylation of tubulin cytoskeleton by SIRT2.
This will compromise autophagy, and thus, the clearance of damaged organelles and protein aggregates.
We envision that targeting mitochondria- and/or SIRT2-associated processes can be a novel promising therapeutic approach for PD pathology.

Dr Yuma Yamada, from Laboratory for Molecular Design of Pharmaceutics, Faculty of Pharmaceutical Sciences, Hokkaido University, Japan was awarded by Ninapharm for his Scientific Contribution and his work about Mitochondrial genome targeting by DF-MITO-Porter via endosomal and mitochondrial membrane fusion.

Dr Yamada's Abstract:

Mitochondrial genetic disorders are known as major cause of mitochondrial diseases. It therefore appears likely that mitochondrial gene therapy will be useful and productive for the treatment of various diseases. To achieve such an innovative strategy targeted mitochondrial genome, it will be necessary to deliver therapeutic agents to mitochondria in living cells. We previously developed a Dual Function MITO-Porter (DF-MITO-Porter), an innovative nano carrier for mitochondrial delivery, which has the ability to pass through endosomal and mitochondrial membranes via step-wise membrane fusion [Ref. 1]. Here, we report that the DF-MITO-Porter has the ability to deliver bioactive molecules into the mitochondrial matrix, which contains mtDNA pool. We first constructed DF-MITO-Porter encapsulating DNase I protein as a model bioactive molecule. It is expected that mtDNA would be digested, when the mitochondrial matrix delivery of DNase I proteins progressed.
We measured the mtDNA-levels after delivery of DNase I protein by DF-MITO-Porter. As results, we confirmed that the mitochondrial delivery of DNase I proteins by DF-MITO-Porter could selectively digest mtDNA, and the results suggest potential use of DF-MITO-Porter in therapies aimed

at mitochondrial genome.

The Education Award was discerned to Dr Gilles Casano, from University of Aix-en-Provence, France. Noxygen Science Transfer & Diagnostics GmBH supported this award.





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