MicroRNAs in Major Depressive Disorder

Fries, Gabriel R.; Zhang, Wei; Benevenuto, Deborah; Quevedo, João

doi:10.1007/978-3-030-05542-4_9

Cited by 27 publications

(15 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MicroRNAs play an important role in psychiatric disorders, especially depression [23,24,25,26]. Samples from peripheral blood including PBMCs, whole blood, serum, and plasma were screened to identify any microRNAs associated with depression.…”

Section: Introductionmentioning

confidence: 99%

Aberrant Expression of Intracellular let-7e, miR-146a, and miR-155 Correlates with Severity of Depression in Patients with Major Depressive Disorder and Is Ameliorated after Antidepressant Treatment

Hung

Tsai

et al. 2019

Cells

View full text Add to dashboard Cite

Chronic inflammation and abnormalities in Toll-like receptor (TLR) signaling pathways are associated with major depressive disorder (MDD). Our previous work reported that impaired negative regulators for the TLR pathways are associated with MDD. This study aimed to assess the association between the severity of depression and the intracellular microRNAs that regulate TLR4 signaling in both peripheral blood mononuclear cells (PBMCs) and monocytes from MDD patients. The severity of MDD before and after antidepressant treatment was determined by the 17-item Hamilton Depression Rating Scale, and quantitative RT-PCR was used to measure the levels of intracellular regulatory microRNAs, including let-7e, miR-21-5p miR-145, miR-223, miR-146a, and miR-155, in PBMCs and monocytes isolated from 43 healthy controls and 84 patients with MDD before and after treatment with antidepressants. Assays of PBMCs showed that the levels of let-7e, miR-146a, and miR-155 were lower in MDD patients than in healthy controls and were significantly higher after than before treatment in the 69 patients who completed treatment with antidepressants for four weeks. Levels of miR-146a and miR-155 in monocytes were lower in MDD patients than in controls and were increased in the former after antidepressant treatment. Multiple linear regression analyses found that let-7e and miR-146a expression before treatment was inversely correlated with severity of depression, whereas miR-155 before treatment was directly correlated with severity of depression. These findings suggest that intracellular regulatory microRNAs which regulate TLR4 signaling are aberrantly expressed in patients with MDD and that these levels are ameliorated by antidepressant treatment.

show abstract

Section: Introductionmentioning

confidence: 99%

Aberrant Expression of Intracellular let-7e, miR-146a, and miR-155 Correlates with Severity of Depression in Patients with Major Depressive Disorder and Is Ameliorated after Antidepressant Treatment

Hung

Tsai

et al. 2019

Cells

View full text Add to dashboard Cite

show abstract

“…The role of small noncoding RNAs (microRNAs, miRNAs) and long noncoding RNAs (lncRNAs) [81] in the aetiology of depressive response is also important. miRNAs can modulate posttranscriptional gene expression by interfering with translation controlled by mRNAs [82]. lncRNAs are highly expressed in the brain and participate in various normal brain functions as well as neuropsychiatric disorders [83].…”

Section: Further Directions Ofmentioning

confidence: 99%

Epigenetic Mechanisms in the Neurodevelopmental Theory of Depression

Talarowska

2020

Depression Research and Treatment

View full text Add to dashboard Cite

The genome (genes), epigenome, and environment work together from the earliest stages of human life to produce a phenotype of human health or disease. Epigenetic modifications, including among other things: DNA methylation, modifications of histones and chromatin structure, as well as functions of noncoding RNA, are coresponsible for specific patterns of gene expression. This refers also to mental disorders, including depressive disorders. Early childhood experiences accompanied by severe stressors (considered a risk factor for depression in adult life) are linked with changes in gene expression. They include genes involved in a response to stress (hypothalamic-pituitary-adrenal axis, HPA), associated with autonomic nervous system hyperactivity and with cortical, and subcortical processes of neuroplasticity and neurodegeneration. These are, among others: gene encoding glucocorticoid receptor, FK506 binding protein 5 gene (FKBP5), gene encoding arginine vasopressin and oestrogen receptor alpha, 5-hydroxy-tryptamine transporter gene (SLC6A4), and gene encoding brain-derived neurotrophic factor. How about personality? Can the experiences unique to every human being, the history of his or her development and gene-environment interactions, through epigenetic mechanisms, shape the features of our personality? Can we pass on these features to future generations? Hence, is the risk of depression inherent in our biological nature? Can we change our destiny?

show abstract

“…10 Numerous studies have revealed the crucial roles of microRNAs in regulating gene expression during the development of brain, synaptic plasticity as well as neuroplasticity and neurogenesis. 11,12 Significant research showed that the dysregulation of miRNAs is involved in different degenerative diseases including Down syndrome, Alzheimer's disease and Parkinson's disease. miRNAs are also extensively involved in depression and stress-related diseases based on evidence from preclinical and clinical studies.…”

Section: Introductionmentioning

confidence: 99%

<p>miR-138 Increases Depressive-Like Behaviors by Targeting SIRT1 in Hippocampus</p>

Li¹,

Wang²,

Pei³

et al. 2020

NDT

View full text Add to dashboard Cite

Background: Major depressive disorder (MDD) is a serious and common mood disorder with unknown etiology. Emerging evidence has demonstrated the critical roles of SIRT1 and microRNAs (miRNAs) in the progression of MDD. However, the underlying molecular mechanisms remain to be fully understood. Methods: In the present study, the expression level of miR-138 and SIRT1 were analyzed by RT-PCR or Western blotting in a chronic unpredictable mild stress (CUMS) model. The depressive-like behaviors were analyzed by forced swimming test (FST) and sucrose preference test (SPT) in mice injected with miR-138 and SIRT1 overexpression lentivirus. The luciferase reporter assay was used to assess the direct regulation of miR-138 on SIRT1 expression. Results: The upregulation of miR-138 was found in the hippocampus of the CUMS mice and correlated with decreased SIRT1 expression. C57BL/6J mice treated with SIRT1-and miR-138-expressing (miR-138) lentivirus showed increased depressive-like behaviors. In contrast, SIRT1 or si-miR-138 lentivirus treated C57BL/6J mice showed decreased depressive-like behaviors. Moreover, the Sirt1/PGC-1α/FNDC5/BDNF pathway was downregulated following miR-138 overexpression and increased upon miR-138 knockdown in hippocampus in CUMS mice and cultured primary neuronal cells. Mechanistically, luciferase reporter assay demonstrated that SIRT1 gene was a downstream transcriptional target of miR-138. Conclusion: Our data demonstrated the regulation role of miR-138 on SIRT1 gene expression, miR-138 increased depressive-like behaviors by regulating SIRT1 expression in hippocampus.

show abstract

MicroRNAs in Major Depressive Disorder

Cited by 27 publications

References 72 publications

Aberrant Expression of Intracellular let-7e, miR-146a, and miR-155 Correlates with Severity of Depression in Patients with Major Depressive Disorder and Is Ameliorated after Antidepressant Treatment

Aberrant Expression of Intracellular let-7e, miR-146a, and miR-155 Correlates with Severity of Depression in Patients with Major Depressive Disorder and Is Ameliorated after Antidepressant Treatment

Epigenetic Mechanisms in the Neurodevelopmental Theory of Depression

<p>miR-138 Increases Depressive-Like Behaviors by Targeting SIRT1 in Hippocampus</p>

Contact Info

Product

Resources

About