Abstract
Objectives: Recent evidences suggest that mitochondrial dysfunction maybe involved in the pathophysiology of major depressive disorder (MDD); however, the role of mitochondrial genes in this disorder has not been studied systematically. In the present study, we profiled expression of mitochondrial genes in dorsolateral prefrontal cortex (dlPFC) of MDD and non-psychiatric control subjects.Methods: Human mitochondrial RT2 profile PCR array plates were used to examine differentially expressed genes in dlPFC of 11 MDD and 11 control subjects. Differentially expressed genes were validated independently by qRT-PCR. Biological relevance of differentially expressed genes was analysed by gene ontology (GO) and ingenuity pathways analysis (IPA).Results: We found that 16 genes were differentially expressed in the MDD group compared with control group. Among them, three genes were downregulated and 13 genes upregulated. None of these genes were affected by confounding variables, such as age, post-mortem interval, brain pH, and antidepressant toxicology. Seven differentially expressed genes were successfully validated in MDD subjects. GO and IPA analyses identified several new regulatory networks associated with mitochondrial dysfunctions in MDD.Conclusions: Our findings suggest abnormal mitochondrial systems in the brain of MDD subjects which could be involved in the etiopathogenesis of this disorder.
Highlights
Major depressive disorder (MDD) is a common psychiatry disorder, the lifetime prevalence of which is 15%~20%
Gene Ontology (GO) and ingenuity pathways analysis (IPA) analyses identified several new regulatory networks associated with mitochondrial dysfunctions in MDD
Our findings suggest abnormal mitochondrial systems in the brain of MDD subjects which could be involved in the etiopathogenesis of this disorder
Summary
Major depressive disorder (MDD) is a common psychiatry disorder, the lifetime prevalence of which is 15%~20%. It is hypothesized that mitochondrial dysfunction in specific brain regions may be related to the cause or effect of MDD (Tobe 2013). Mitochondria are vital cellular organelles, which generate adenosine triphosphate (ATP) via mitochondrial respiratory chain (oxidative phosphorylation) in eukaryotic cells. ATP acts as the universal energy used for a wide range of cellular process (Perier and Vila 2012). That is why neuron related diseases are highly vulnerable to mitochondrial dysfunction (Ivanov et al 2014). Besides acting as a power station, mitochondrial dynamics regulate neuronal energy metabolism, Ca2+ homeostasis, and dendritic and axonal motility, which affect release of neurotransmitters and neurotropic factors (Mattson et al 2008)
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