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10.1038/cddis.2014.581 http://scihub22266oqcxt.onion/10.1038/cddis.2014.581 C4669776!4669776 !25611391     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25611391 &cmd=llinks): Failed to open stream: HTTP request failed! 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PINK1-induced mitophagy promotes neuroprotection in Huntington s disease |pdf=|usr=}}{{25611391 }} gab.com Text PINK1-induced mitophagy promotes neuroprotection in Huntington s disease JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=25611391 #FOAvip Huntington's disease (HD) is a fatal neurodegenerative disorder caused by aberrant expansion of CAG repeat in the huntingtin gene. Mutant Huntingtin (mHtt) alters multiple cellular processes, leading to neuronal dysfunction and death. Among those alterations, impaired mitochondrial metabolism seems to have a major role in HD pathogenesis. In this study, we used the Drosophila model system to further investigate the role of mitochondrial damages in HD. We first analyzed the impact of mHtt on mitochondrial morphology, and surprisingly, we revealed the formation of abnormal ring-shaped mitochondria in photoreceptor neurons. Because such mitochondrial spheroids were previously detected in cells where mitophagy is blocked, we analyzed the effect of PTEN-induced putative kinase 1 (PINK1), which controls Parkin-mediated mitophagy. Consistently, we found that PINK1 overexpression alleviated mitochondrial spheroid formation in HD flies. More importantly, PINK1 ameliorated ATP levels, neuronal integrity and adult fly survival, demonstrating that PINK1 counteracts the neurotoxicity of mHtt. This neuroprotection was Parkin-dependent and required mitochondrial outer membrane proteins, mitofusin and the voltage-dependent anion channel. Consistent with our observations in flies, we demonstrated that the removal of defective mitochondria was impaired in HD striatal cells derived from HdhQ111 knock-in mice, and that overexpressing PINK1 in these cells partially restored mitophagy. The presence of mHtt did not affect Parkin-mediated mitochondrial ubiquitination but decreased the targeting of mitochondria to autophagosomes. Altogether, our findings suggest that mitophagy is altered in the presence of mHtt and that increasing PINK1/Parkin mitochondrial quality control pathway may improve mitochondrial integrity and neuroprotection in HD. Twit Text FOAVip PINK1-induced mitophagy promotes neuroprotection in Huntington s disease ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=25611391 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25611391 #FOAvip English Wikipedia <ref>{{Cite pmid|25611391 }}</ref> PINK1-induced mitophagy promotes neuroprotection in Huntington s disease #MMPMID25611391 Khalil B ; El Fissi N ; Aouane A ; Cabirol-Pol MJ ; Rival T ; Liévens JC Cell Death Dis 2015[Jan]; 6 (1 ): e1617 PMID25611391 show ga Huntington's disease (HD) is a fatal neurodegenerative disorder caused by aberrant expansion of CAG repeat in the huntingtin gene. Mutant Huntingtin (mHtt) alters multiple cellular processes, leading to neuronal dysfunction and death. Among those alterations, impaired mitochondrial metabolism seems to have a major role in HD pathogenesis. In this study, we used the Drosophila model system to further investigate the role of mitochondrial damages in HD. We first analyzed the impact of mHtt on mitochondrial morphology, and surprisingly, we revealed the formation of abnormal ring-shaped mitochondria in photoreceptor neurons. Because such mitochondrial spheroids were previously detected in cells where mitophagy is blocked, we analyzed the effect of PTEN-induced putative kinase 1 (PINK1), which controls Parkin-mediated mitophagy. Consistently, we found that PINK1 overexpression alleviated mitochondrial spheroid formation in HD flies. More importantly, PINK1 ameliorated ATP levels, neuronal integrity and adult fly survival, demonstrating that PINK1 counteracts the neurotoxicity of mHtt. This neuroprotection was Parkin-dependent and required mitochondrial outer membrane proteins, mitofusin and the voltage-dependent anion channel. Consistent with our observations in flies, we demonstrated that the removal of defective mitochondria was impaired in HD striatal cells derived from HdhQ111 knock-in mice, and that overexpressing PINK1 in these cells partially restored mitophagy. The presence of mHtt did not affect Parkin-mediated mitochondrial ubiquitination but decreased the targeting of mitochondria to autophagosomes. Altogether, our findings suggest that mitophagy is altered in the presence of mHtt and that increasing PINK1/Parkin mitochondrial quality control pathway may improve mitochondrial integrity and neuroprotection in HD. |*Mitophagy [MESH] |Animals [MESH] |Drosophila Proteins/metabolism [MESH] |Drosophila melanogaster/*metabolism [MESH] |Eye/pathology/ultrastructure [MESH] |Huntington Disease/*metabolism/*pathology [MESH] |Mice [MESH] |Mitochondria/metabolism/ultrastructure [MESH] |Mutant Proteins/metabolism [MESH] |Neostriatum/metabolism/pathology [MESH] |Nerve Degeneration/pathology [MESH] |Neurons/metabolism/pathology/ultrastructure [MESH] |Neuroprotective Agents/*metabolism [MESH] |Phagosomes/metabolism/ultrastructure [MESH] |Protein Kinases/*metabolism [MESH] |Serotonin Plasma Membrane Transport Proteins/metabolism [MESH] |Spheroids, Cellular/metabolism [MESH] |Survival Analysis [MESH]PINK1-induced mitophagy promotes neuroprotection in Huntington s disea(epmc).pdf DeepDyve Pubget Overpricing