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BNIP3L/NIX-mediated mitophagy protects against glucocorticoid-induced synapse defects
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BNIP3L/NIX-mediated mitophagy protects against glucocorticoid-induced synapse defects
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Journal Article
BNIP3L/NIX-mediated mitophagy protects against glucocorticoid-induced synapse defects
2021
Overview
Stress-induced glucocorticoids disturb mitochondrial bioenergetics and dynamics; however, instead of being removed via mitophagy, the damaged mitochondria accumulate. Therefore, we investigate the role of glucocorticoids in mitophagy inhibition and subsequent synaptic defects in hippocampal neurons, SH-SY5Y cells, and ICR mice. First, we observe that glucocorticoids decrease both synaptic density and vesicle recycling due to suppressed mitophagy. Screening data reveal that glucocorticoids downregulate BNIP3-like (BNIP3L)/NIX, resulting in the reduced mitochondrial respiration function and synaptic density. Notably, we find that glucocorticoids direct the glucocorticoid receptor to bind directly to the PGC1α promoter, downregulating its expression and nuclear translocation. PGC1α downregulation selectively decreases NIX-dependent mitophagy. Consistent with these results, NIX enhancer pre-treatment of a corticosterone-exposed mouse elevates mitophagy and synaptic density in hippocampus, improving the outcome of a spatial memory task. In conclusion, glucocorticoids inhibit mitophagy via downregulating NIX and that NIX activation represents a potential target for restoring synapse function.
Stress-induced glucocorticoids cause mitochondrial damage in neurons, but they are not cleared by mitophagy. Here, the authors show that glucocorticoids inhibit NIX-dependent basal mitophagy, contributing to neurodegeneration in a mouse model that can be reversed by pretreatment with a NIX enhancer.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 14/1
/ 14/35
/ 38/39
/ 38/44
/ 38/77
/ 64/60
/ 82/51
/ 96
/ 96/31
/ Animals
/ Corticosterone - pharmacology
/ Defects
/ Density
/ Glucocorticoids - adverse effects
/ Hormones
/ Humanities and Social Sciences
/ Hydrocortisone - pharmacology
/ Male
/ Membrane Proteins - genetics
/ Membrane Proteins - metabolism
/ Memory
/ Mice
/ Mitochondrial Proteins - genetics
/ Mitochondrial Proteins - metabolism
/ Neuronal Plasticity - physiology
/ Neurons
/ Protective Agents - metabolism
/ Protein Kinases - metabolism
/ Science
/ Synapses
