scholarly journals Mitochondrial gene signature in the prefrontal cortex for differential susceptibility to chronic stress

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Meltem Weger ◽  
Daniel Alpern ◽  
Antoine Cherix ◽  
Sriparna Ghosal ◽  
Jocelyn Grosse ◽  
...  

Abstract Mitochondrial dysfunction was highlighted as a crucial vulnerability factor for the development of depression. However, systemic studies assessing stress-induced changes in mitochondria-associated genes in brain regions relevant to depression symptomatology remain scarce. Here, we performed a genome-wide transcriptomic study to examine mitochondrial gene expression in the prefrontal cortex (PFC) and nucleus accumbens (NAc) of mice exposed to multimodal chronic restraint stress. We identified mitochondria-associated gene pathways as most prominently affected in the PFC and with lesser significance in the NAc. A more detailed mitochondrial gene expression analysis revealed that in particular mitochondrial DNA-encoded subunits of the oxidative phosphorylation complexes were altered in the PFC. The comparison of our data with a reanalyzed transcriptome data set of chronic variable stress mice and major depression disorder subjects showed that the changes in mitochondrial DNA-encoded genes are a feature generalizing to other chronic stress-protocols as well and might have translational relevance. Finally, we provide evidence for changes in mitochondrial outputs in the PFC following chronic stress that are indicative of mitochondrial dysfunction. Collectively, our work reinforces the idea that changes in mitochondrial gene expression are key players in the prefrontal adaptations observed in individuals with high behavioral susceptibility and resilience to chronic stress.

2020 ◽  
Author(s):  
Yue Liu ◽  
Shuai Yang ◽  
Wei Zhang ◽  
Yan Yang ◽  
Ming Jiang ◽  
...  

Abstract Background: Mitochondrial dysfunction is linked to the etiopathogenesis of postoperative delirium (POD), which severely affects the prognosis of elderly patients undergoing surgery. The methylation of mitochondrial DNA (mtDNA), a new and incompletely described phenomenon that regulates the structure and function of mitochondria, is associated with aging. However, the relationship between mtDNA methylation and POD has not been established. Methods: 5-methylcytosine (5-mC) at 5 CpG sites of the displacement loop (D-loop) and at 60 CpG sites of coding gene loci in the mitochondrial genome after surgery of the hippocampus, prefrontal cortex, amygdala, and anterior cingulate cortex in 6- and 18-month-old mice were detected using bisulfite pyrosequencing. Mitochondrial structure, mitochondrial gene expression and mtDNA copy number were also examined using Electron microscopy and real time PCR to find the association with mtDNA methylationResults: The mtDNA methylation drift manifested as a decrease in the methylation levels at the D-loop and an increase or decrease in the methylation levels at several coding gene loci, ultimately resulting in reduced mtDNA copy numbers, altered mitochondrial gene expression, and damaged mitochondrial structures in the hippocampus and prefrontal cortex after surgery. The activation of Silent information regulator-1 (SIRT1) ameliorated anesthesia- and surgery-induced mitochondrial dysfunction and delirium-like behaviors by regulating mtDNA methyltransferase-mediated mtDNA methylation. Conclusions: These data support the existence of epigenetic mtDNA regulation in POD; however, further studies are required to explore the specific mechanisms.


1992 ◽  
Vol 5 (1) ◽  
pp. 13-26 ◽  
Author(s):  
G. Spangenberg ◽  
R. P�rez Vicente ◽  
M. M. Oliveira ◽  
M. Osusky ◽  
J. Nagel ◽  
...  

2011 ◽  
Vol 39 (18) ◽  
pp. 8029-8041 ◽  
Author(s):  
Inge Kühl ◽  
Laurent Dujeancourt ◽  
Mauricette Gaisne ◽  
Christopher J. Herbert ◽  
Nathalie Bonnefoy

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