Epigenetic mechanisms of stress and depression

Chmielewska, Natalia; Szyndler, Janusz; Maciejak, Piotr; Płaźnik, Adam

doi:10.12740/pp/94375

Cited by 29 publications

(20 citation statements)

References 56 publications

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“…One potential mechanism by which PMS has a sustained effect on ASIC1 expression and visceral sensitivity is an epigenetic regulation of gene expression 39 . Epigenetic factors such as DNA methylation, histone acetylation, and miRNAs are all reflections of changes in environmental stimuli 40,41 . MiRNA, a small RNA sequence, can play a major role in cell differentiation, biological development, and disease development by directly inhibiting target gene translation 42,43 .…”

Section: Discussionmentioning

confidence: 99%

“…39 Epigenetic factors such as DNA methylation, histone acetylation, and miRNAs are all reflections of changes in environmental stimuli. 40,41 MiRNA, a small RNA sequence, can play a major role in cell differentiation, biological development, and disease development by directly inhibiting target gene translation. 42,43 Recent years, there were literatures reported the roles of miRNAs in a variety of pregnancy-related complications such as preeclampsia and FGR, indicating its importance in pregnancy.…”

Section: Discussionmentioning

confidence: 99%

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Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress

Xue

et al. 2020

CNS Neurosci Ther

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Aims Irritable bowel syndrome (IBS) is a common functional gastrointestinal disease characterized by abdominal pain. Our recent study has shown that the acid‐sensitive ion channel 1 (ASIC1) in dorsal root ganglion (DRG) is involved in stomachache of adult offspring rats subjected with prenatal maternal stress (PMS). MiR‐485 is predicted to target the expression of ASIC1. The aim of the present study was designed to determine whether miR‐485/ASIC1 signaling participates in enterodynia in the spinal dorsal horn of adult offspring rats with PMS. Methods Enterodynia was measured by colorectal distension (CRD). Western blotting, qPCR, and in situ hybridization were performed to detect the expression of ASICs and related miRNAs. Spinal synaptic transmission was also recorded by patch clamping. Results PMS offspring rats showed that spinal ASIC1 protein expression and synaptic transmission were significantly enhanced. Administration of ASICs antagonist amiloride suppressed the synaptic transmission and enterodynia. Besides, PMS induced a significant reduction in the expression of miR‐485. Upregulating the expression markedly attenuated enterodynia, reversed the increase in ASIC1 protein and synaptic transmission. Furthermore, ASIC1 and miR‐485 were co‐expressed in NeuN‐positive spinal dorsal horn neurons. Conclusions Overall, these data suggested that miR‐485 participated in enterodynia in PMS offspring, which is likely mediated by the enhanced ASIC1 activities.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress

Xue

et al. 2020

CNS Neurosci Ther

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“…Lastly, platelet serotonin might not only be important in platelet activation and subsequent involvement in platelet-related pathologies that are co-morbid with MDD, but also for its role as an epigenetic modulator in the serotonylation, a covalent posttranslational modification occurring at the level of histones thereby influencing gene expression [317]. Indeed, epigenetics has been hypothesized to play a major role in the etiology of depression [318][319][320]. In this view, serotonylation could represent a platelet-mediated link between serotonin and depression onset, a hypothesis which warrants further investigation.…”

Section: Discussionmentioning

confidence: 99%

Beyond Haemostasis and Thrombosis: Platelets in Depression and Its Co-Morbidities

Izzi

Tirozzi

Cerletti

et al. 2020

IJMS

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Alongside their function in primary haemostasis and thrombo-inflammation, platelets are increasingly considered a bridge between mental, immunological and coagulation-related disorders. This review focuses on the link between platelets and the pathophysiology of major depressive disorder (MDD) and its most frequent comorbidities. Platelet- and neuron-shared proteins involved in MDD are functionally described. Platelet-related studies performed in the context of MDD, cardiovascular disease, and major neurodegenerative, neuropsychiatric and neurodevelopmental disorders are transversally presented from an epidemiological, genetic and functional point of view. To provide a complete scenario, we report the analysis of original data on the epidemiological link between platelets and depression symptoms suggesting moderating and interactive effects of sex on this association. Epidemiological and genetic studies discussed suggest that blood platelets might also be relevant biomarkers of MDD prediction and occurrence in the context of MDD comorbidities. Finally, this review has the ambition to formulate some directives and perspectives for future research on this topic.

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“…Early and adult stress exposure is related to epigenetic changes in genes related to mood regulation, for example, participation Genes that regulate hypothalamic-pituitary-adrenal axis activity (NR3C1) or genes responsible for serotonin transporter (5-HTT)-encoding gene SLC6A4 (Wang et al, 2020). Data from epigenetic studies indicate that the mechanism of action of certain antidepressants (such as fluoxetine and escitalopram) or mood stabilizers (such as valproic acid) are at least partially related to epigenetic processes (Chmielewska et al, 2019). The association between early life stress and depression is controlled by genetic risk factors, including serotonin transporter, brain derived neurotrophic factor, glucocorticoid receptor, FK506-binding protein 5 and corticotropin releasing hormone receptor 1 polymorphisms.…”

Section: Changes Caused By Early Life Stressmentioning

confidence: 99%

Early Life Stress Induced DNA Methylation of Monoamine Oxidases Leads to Depressive-Like Behavior

Jiang

et al. 2020

Front. Cell Dev. Biol.

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Major depressive disorder (MDD) is coming to be the regarded as one of the leading causes for human disabilities. Due to its complicated pathological process, the etiology is still unclear and the treatment is still targeting at the monoamine neurotransmitters. Early life stress has been known as a major cause for MDD, but how early life stress affects adult monoaminergic activity is not clear either. Recently, DNA methylation is considered to be the key mechanism of epigenetics and might play a role in early life stress induced mental illness. DNA methylation is an enzymatic covalent modification of DNA, has been one of the main epigenetic mechanisms investigated. The metabolic enzyme for the monoamine neurotransmitters, monoamine oxidases A/B (MAO A/MAO B) are the prime candidates for the investigation into the role of DNA methylation in mental disorders. In this review, we will review recent advances about the structure and physiological function of monoamine oxidases (MAO), brief narrative other factors include stress induced changes, early life stress, perinatal depression (PD) relationship with other epigenetic changes, such as DNA methylation, microRNA (miRNA). This review will shed light on the epigenetic changes involved in MDD, which may provide potential targets for future therapeutics in depression pathogenesis.

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Epigenetic mechanisms of stress and depression

Cited by 29 publications

References 56 publications

Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress

Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress

Beyond Haemostasis and Thrombosis: Platelets in Depression and Its Co-Morbidities

Early Life Stress Induced DNA Methylation of Monoamine Oxidases Leads to Depressive-Like Behavior

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