View source for Van Den Brink 2018 PLoS Genet

{{Publication
|title=Van Den Brink DM, Cubizolle A, Chatelain G, Davoust N, Girard V, Johansen S, Napoletano F, Dourlen P, Guillou L, Angebault-Prouteau C, Bernoud-Hubac N, Guichardant M, Brabet P, Mollereau B (2018) Physiological and pathological roles of FATP-mediated lipid droplets in Drosophila and mice retina. PLoS Genet 14:e1007627.
|info=[https://www.ncbi.nlm.nih.gov/pubmed/30199545 PMID: 30199545 Open Access]
|authors=Van Den Brink DM, Cubizolle A, Chatelain G, Davoust N, Girard V, Johansen S, Napoletano F, Dourlen P, Guillou L, Angebault-Prouteau C, Bernoud-Hubac N, Guichardant M, Brabet P, Mollereau B
|year=2018
|journal=PLoS Genet
|abstract=Increasing evidence suggests that dysregulation of lipid metabolism is associated with neurodegeneration in retinal diseases such as age-related macular degeneration and in brain disorders such as Alzheimer's and Parkinson's diseases. Lipid storage organelles (lipid droplets, LDs), accumulate in many cell types in response to stress, and it is now clear that LDs function not only as lipid stores but also as dynamic regulators of the stress response. However, whether these LDs are always protective or can also be deleterious to the cell is unknown. Here, we investigated the consequences of LD accumulation on retinal cell homeostasis under physiological and stress conditions in ''Drosophila'' and in mice. In wild-type ''Drosophila'', we show that ''dFatp'' is required and sufficient for expansion of LD size in retinal pigment cells (RPCs) and that LDs in RPCs are required for photoreceptor survival during aging. Similarly, in mice, LD accumulation induced by RPC-specific expression of human FATP1 was non-toxic and promoted mitochondrial energy metabolism in RPCs and non-autonomously in photoreceptor cells. In contrast, the inhibition of LD accumulation by ''dFatp'' knockdown suppressed neurodegeneration in ''Aats-met<sup>FB</sup>'' Drosophila mutants, which carry elevated levels of reactive oxygen species (ROS). This suggests that abnormal turnover of LD may be toxic for photoreceptors cells of the retina under oxidative stress. Collectively, these findings indicate that FATP-mediated LD formation in RPCs promotes RPC and neuronal homeostasis under physiological conditions but could be deleterious for the photoreceptors under pathological conditions.
|editor=[[Plangger M]],
}}
{{Labeling
|area=Respiration, Genetic knockout;overexpression
|diseases=Neurodegenerative
|organism=Mouse
|tissues=Endothelial;epithelial;mesothelial cell
|preparations=Permeabilized cells
|enzymes=TCA cycle and matrix dehydrogenases
|couplingstates=LEAK, OXPHOS
|pathways=F, N, S, NS
|instruments=Oxygraph-2k
|additional=Labels, 2018-10,
}}