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Risiglione 2022 Life (Basel)

From Bioblast
Publications in the MiPMap
Risiglione P, Cubisino SAM, Lipari CLR, De Pinto V, Messina A, Magrì A (2022) α-Synuclein A53T promotes mitochondrial proton gradient dissipation and depletion of the organelle respiratory reserve in a neuroblastoma cell line.

» Life (Basel) 12:894. PMID: 35743925 Open Access

Risiglione Pierpaolo,  Cubisino Salvatore Antonio Maria, Lipari Cristiana Lucia Rita,  De Pinto Vito, Messina Angela, Magri Andrea (2022) Life (Basel)

Abstract: α-synuclein (αSyn) is a small neuronal protein whose accumulation correlates with Parkinson's disease. αSyn A53T mutant impairs mitochondrial functions by affecting substrate import within the organelle, activity of complex I and the maximal respiratory capacity. However, the precise mechanism initiating the bioenergetic dysfunction is not clearly understood yet. By overexpressing αSyn A53T in SH-SY5Y cells, we investigated the specific changes in the mitochondrial respiratory profile using High-Resolution Respirometry. We found that αSyn A53T increases dissipative fluxes across the intermembrane mitochondrial space: this does not compromise the oxygen flows devoted to ATP production while it reduces the bioenergetic excess capacity of mitochondria, providing a possible explanation of the increased cell susceptibility observed in the presence of further stress stimuli. Keywords: Parkinson’s disease, High-resolution respirometry, Mitochondrial dysfunction, αSyn Bioblast editor: Plangger M O2k-Network Lab: IT Catania Messina A

Labels: MiParea: Respiration, Genetic knockout;overexpression  Pathology: Parkinson's 

Organism: Human  Tissue;cell: Neuroblastoma  Preparation: Permeabilized cells, Intact cells 

Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: N, S, NS, ROX  HRR: Oxygraph-2k