Mitochondrial DNA copy number, damage, repair and degradation in depressive disorder

Czarny, Piotr; Wigner, Paulina; Strycharz, Justyna; Świderska, Ewa; Synowiec, Ewelina; Szatkowska, Magdalena; Śliwińska, Agnieszka; Talarowska, Monika; Szemraj, Janusz; Su, Kuan‐Pin; Maes, Michaël; Śliwiński, Tomasz; Gałecki, Piotr

doi:10.1080/15622975.2019.1588993

Cited by 22 publications

(17 citation statements)

References 79 publications

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“…In BD, a meta-analysis for BD-mtDNA copy number studies with a low level of heterogeneity revealed a significant lower mtDNA copy number in patients ( 154 ). In contrast, another meta-analysis with a higher level of heterogeneity identified no significant differences between mtDNA copy numbers in BD patients.…”

Section: Overview and Discussionmentioning

confidence: 99%

“…Moreover, a recent study found a higher mtDNA copy number and a decreased DNA methylation status in the peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC1α) promoter in patients with MDD, which leads to reduced expression of mitochondrial genes (2,152). In contrast, Czarny et al (153) showed that the cellular mtDNA copy number did not differ between healthy and depressed subjects, but it showed a lower capacity for degradation and a higher number of lesions compared to controls (154).…”

Section: Genetic Changesmentioning

confidence: 97%

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The Role of Mitochondria in Mood Disorders: From Physiology to Pathophysiology and to Treatment

et al. 2021

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Mitochondria are cellular organelles involved in several biological processes, especially in energy production. Several studies have found a relationship between mitochondrial dysfunction and mood disorders, such as major depressive disorder and bipolar disorder. Impairments in energy production are found in these disorders together with higher levels of oxidative stress. Recently, many agents capable of enhancing antioxidant defenses or mitochondrial functioning have been studied for the treatment of mood disorders as adjuvant therapy to current pharmacological treatments. A better knowledge of mitochondrial physiology and pathophysiology might allow the identification of new therapeutic targets and the development and study of novel effective therapies to treat these specific mitochondrial impairments. This could be especially beneficial for treatment-resistant patients. In this article, we provide a focused narrative review of the currently available evidence supporting the involvement of mitochondrial dysfunction in mood disorders, the effects of current therapies on mitochondrial functions, and novel targeted therapies acting on mitochondrial pathways that might be useful for the treatment of mood disorders.

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Section: Overview and Discussionmentioning

confidence: 99%

Section: Genetic Changesmentioning

confidence: 97%

The Role of Mitochondria in Mood Disorders: From Physiology to Pathophysiology and to Treatment

et al. 2021

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“…The goodness of fit of logistic regression models showing a significant degree of discrimination between controls and patients was estimated with Hosmer-Lemeshow test. Efficiency of the treatment was calculated using the formula as described before (Czarny et al, 2019):…”

Section: Discussionmentioning

confidence: 99%

Novel association between TGFA, TGFB1, IRF1, PTGS2 and IKBKB single-nucleotide polymorphisms and occurrence, severity and treatment response of major depressive disorder

Białek

Czarny

Watała

et al. 2020

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Background Activation of the immune system might affect the severity of depressive episodes as well as response to the antidepressant treatment. The purpose of this study was to investigate whether the occurrence of variant alleles of analyzed SNPs are involved in prevalence and progression of depression. Moreover, selected genes and SNPs have not been investigated in context of the disease severity and treatment. Therefore, six polymorphisms were selected: g.41354391A>G-TGFB1 (rs1800469), g.132484229C>A-IRF (rs2070729), g.186643058A>G-PTGS2 (rs5275), g.186640617C>T-PTGS2 (rs4648308), g.70677994G>A-TGFA (rs2166975) and g.42140549G>T–IKBKB (rs5029748). Methods A total of 360 (180 patients and 180 controls) DNA samples were genotyped using TaqMan probes. Results We observed that A/G of the rs2166975 TGFA, A/C of rs2070729 IRF1 and G/T of rs5029748 IKBKB were associated with an increased risk of depression development while the T/T of rs5029748 IKBKB, T/T of rs4648308 PTGS2 and G/G of rs2166975 TGFA reduced this risk. We also stratified the study group according to gender and found that genotype A/G and allele G of the rs2166975 TGFA, G/T of rs5029748 IKBKB as well as C allele of rs4648308 PTGS2, homozygote A/A and allele A of rs5275 PTGS2 were associated with increased risk of depression development in men while homozygote G/G of rs5275 PTGS2 decreased this risk. Moreover, C/T of rs4648308 PTGS2 and A/G of rs5275 PTGS2 was positively correlated with the risk of the disease occurrence in women. Furthermore, a gene–gene analysis revealed a link between studied polymorphisms and depression. In addition, A/A of rs1800469 TGFB1 was associated with earlier age of onset of the disease while G/G of this SNP increased severity of the depressive episode. Interestingly, A/C of rs2070729 IRF1 and T/T of rs5029748 IKBKB may modulate the effectiveness of selective serotonin reuptake inhibitors therapy. In conclusion, studied SNPs may modulate the risk of occurrence, age of onset, severity of the disease and response to the antidepressant treatment.

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“…In the present study, each group was treated as an independent sample (not paired samples), and the expression level of smooth muscle markers in EGJ smooth muscles and cells cultured in vitro was not clear. The purpose of the present study was to clarify the characteristics of the expression levels of smooth muscle markers in EGJ smooth muscles and cells cultured in vitro, rather than to standardize or homogenize them to compare the expression level of one gene to the others, so there was no blank control group and the fold change in expression of each gene was calculated using the 2 -ΔΔCq method (24)(25)(26), with GAPDH as an internal control. Primer information is presented in Table II.…”

Section: Rt-qpcrmentioning

confidence: 99%

Enzyme‑injected method of enzymatic dispersion at low temperature is effective for isolation of smooth muscle cells from human esophagogastric junction

et al. 2020

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The present study was conducted to examine the feasibility of in vitro isolation and primary culture of smooth muscle cells (SMCs) from the esophagogastric junction (EGJ).Smooth muscles of EGJ were harvested from 23 patients with esophageal cancer during esophagostomy from January 2015 to December 2017. Enzymatic dispersion (ED) was performed for isolation. Collagenase II and Trypsin/EDTA were applied by enzyme injection (EI) into tissue fragments or immersion of tissue fragments into enzyme solution. Growth characteristics and proliferation [Cell Counting Kit-8 (CCK-8)] of cells were recorded for both smooth muscle cell medium (SMCM) and DMEM/F12 containing 10% newborn bovine serum (10%-F12). All ED methods could isolate primary cells; EI was the most effective method with low collagenase II concentration (0.5 mg/ml) at 4˚C for 14-24 h. Primary cells demonstrated mainly spindle-and long-spindle-shaped with 'hills and valleys' morphology. The CCK-8 assay in SMCM showed better proliferation results than in 10%-F12. After passaging for 4-8 generations in SMCM or 2-4 generations in 10%-F12, cells enlarged gradually with passages and lost spindle structures. mRNA and proteins of α-smooth muscle actin (α-SMA), smooth muscle 22 α (SM22α), vimentin, desmin, CD90 and proliferating cell nuclear antigen were detected in tissues and cells with different levels of expression. SMCs of esophageal circular muscle, esophageal longitudinal muscle, gastric circular muscle near sling in gastric bottom and gastric circular muscle near clasp in lesser gastric curvature, all cultured in 10%-F12, exhibited superior smooth muscle phenotypes compared with SMCs cultured in SMCM in terms of α-SMA, SM22α and vimentin expression. The EI method of ED at low temperature appears effective for isolation and primary culture of SMCs from human EGJ in vitro.

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Mitochondrial DNA copy number, damage, repair and degradation in depressive disorder

Cited by 22 publications

References 79 publications

The Role of Mitochondria in Mood Disorders: From Physiology to Pathophysiology and to Treatment

The Role of Mitochondria in Mood Disorders: From Physiology to Pathophysiology and to Treatment

Novel association between TGFA, TGFB1, IRF1, PTGS2 and IKBKB single-nucleotide polymorphisms and occurrence, severity and treatment response of major depressive disorder

Enzyme‑injected method of enzymatic dispersion at low temperature is effective for isolation of smooth muscle cells from human esophagogastric junction

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