Abstract
Purpose: To explore the effect of miR-195a on nerve cells in the hippocampal region of depressionmodel mice.Methods: A chronic social defeat stress (CSDS) model was used as a depressed mouse model. In vivo, C57BL/6J mice received CSDS treatment or miR-195a antagomir. Depression-like behaviors were evaluated. In vitro, the target relationship between miR-195a and brain-derived neurotrophic factor (BDNF) was validated by luciferase reporter assays in HEK-293 cells. In primary cortical neurons, expression levels of miR-195a and BDNF mRNA were evaluated using quantitative polymerase chain reaction (qPCR). BDNF protein expression was determined by western blotting.Results: The sucrose preference ratio and social contact of the CSDS group were significantly decreased, whereas the immobility time was significantly increased, compared with the control group (p< 0.05). Interestingly, the expression of miR-195a was upregulated in the CSDS group compared with control group (p < 0.05). Bioinformatics prediction and luciferase reporter assay data indicate that miR195a bound the BDNF 3’ untranslated region. BDNF protein expression levels were significantly reduced by miR-195a mimic but increased by miR-195a inhibitor, compared with the negative control mimic group (p < 0.05). In vivo, miR-195a antagomir alleviated depression-like behaviors compared with CSDS group. In addition, miR-195a antagomir restored the expression of BDNF in mouse hippocampus in the CSDS group (p < 0.05).Conclusion: MiR-195a inhibitor ameliorates depression-like behaviors of depressed mice by downregulation of BDNF, whereas upregulation of miR-195a inhibits BDNF expression in mouse hippocampus and may contribute to depression.
 Keywords: Chronic social defeat stress, Depression, MiR-195, brain-derived neurotrophic factor, BDNF
Highlights
Depression is a neurological and psychiatric disease caused by multiple factors
Mice show a longer immobility time. These results indicated that the mice in the chronic social defeat stress (CSDS) group exhibited depression-like behaviors
Similar results were found for protein expression level (Figure 2 F). These results suggest that brain-derived neurotrophic factor (BDNF) is a target gene of mir-195a and that it is regulated by mir-195a expression level
Summary
Depression is a neurological and psychiatric disease caused by multiple factors. Patients with depression show persistent low mood and cognitive dysfunction [1]. Studies have shown that mir-195 is upregulated in the brains of suicidal individuals [6]. It is unknown whether mir-195 is associated with depression. A growing body of research has shown that the onset of depression is associated with reduced levels of brain-derived neurotrophic factor (BDNF) [7]. Studies have shown that the number of neurons in depressed mice is significantly reduced, and insufficient or continuous decrease in BDNF content is an important cause of neuronal injury and apoptosis [11]. After verification by DNA sequencing, the plasmids (with or without miR-195a mimic) were transfected into HEK-293 cells using Lipofectamine 3000 (Invitrogen) according to the manufacturer's instructions. A value of p < 0.05 was considered statistically significant
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