Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

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. https://doi.org/10.3390/life12060894

» 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


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 

2022-11