Vascular Endothelial Growth Factor-dependent Spinogenesis Underlies Antidepressant-like Effects of Enriched Environment

Huang, Yu Fei; Yang, Chih Hao; Huang, Chiung Chun

doi:10.1074/jbc.m112.392076

Cited by 29 publications

(16 citation statements)

References 87 publications

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“…clinically, it has been reported that miR-107 levels are reduced in the temporal cortical gray matter during the early stages of Ad progression (18). Furthermore, the overexpression of miR-107 in the hippocampus exhibits antidepressant-like effects (32). consistent with the results of a previous study (17), the present study demonstrated that miR-107 expression was reduced in an Ad model induced by administration of Aβ.…”

Section: Discussionsupporting

confidence: 91%

MicroRNA-107 prevents amyloid-β-induced neurotoxicity and memory impairment in mice

Shu

Zhang

et al. 2017

Int J Mol Med

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The pathogenesis of Alzheimer's disease (AD) has still not been fully elucidated, however it is thought that the build up of amyloid plaque at least partially causes the symptoms of AD. MicroRNAs (miRNAs) are endogenous non‑coding small RNA molecules that regulate the expression and degradation of proteins. The present study induced symptoms of AD in mice via intraventricular injection of amyloid‑β 1‑42 (Aβ1‑42), which decreased levels of miR‑107. However, miR‑107 levels increased following administration of miR‑107 mimic, a double‑stranded RNA molecule designed to imitate the native miRNA. Intraventricular injection of Aβ1‑42 aggregates led to spatial memory impairments, inhibited hippocampal long‑term potentiation (LTP) and resulted in the loss of pyramidal cells in the CA1 region of the hippocampus. The miR‑107 mimic reversed the impairments of spatial memory and LTP and the loss of pyramidal neurons caused by Aβ neurotoxicity. Furthermore, the miR‑107 mimic reversed the Aβ‑induced increase in Aβ1‑42 and phosphorylated Tau levels. Critically, Aβ1‑42 injection decreased levels of brain‑derived neurotrophic factor and reduced the phosphorylation of tyrosine receptor kinase B and protein kinase B; these changes were reversed following treatment with the miR‑107 mimic. Collectively, these results demonstrated that miR‑107 may be a potential target for the treatment of AD.

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Section: Discussionsupporting

confidence: 91%

MicroRNA-107 prevents amyloid-β-induced neurotoxicity and memory impairment in mice

Shu

Zhang

et al. 2017

Int J Mol Med

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“…The neuronal cultures at 12–13 DIV were co-transfected with 2 μg EGFP-β-actin plasmid and 2 μg GFP-SESTD1, GFP-SEC14, GFP-SPEC1, GFP-SPEC2, UXIE, SESTD1, Rac1-CA, GFP-Trio8 (1188–1814), sh-SESTD1-I or sh-DsRed plasmid by Lipofectamine 2000 (Invitrogen) according to the manufacturer’s instructions and determined at 17 DIV. The efficiency of co-transfection can be close to 100% as previously described 40 42 .…”

Section: Methodsmentioning

confidence: 81%

“…In some experiments, to validate SESTD1 protein expression and the specificity of anti-SESTD1 antibody, a lentiviral vector (UXIE) for production of viral particles with bicistronic expression of transgenes and EGFP under the control of ubiquitin promoter and separated by an internal ribosomal entry site was used for generating the full-length SESTD1 as described previously 40 .…”

Section: Methodsmentioning

confidence: 99%

The phospholipid-binding protein SESTD1 negatively regulates dendritic spine density by interfering with Rac1-Trio8 signaling pathway

Lee

Huang

2015

Sci Rep

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Dendritic spines are actin-rich protrusions from neuronal dendrites that harbor the majority of excitatory synapses. The balance of spine formation and retraction may influence dendritic integrity. While knowledge of the molecular mechanisms that promote dendritic spine formation has accumulated, little is known about the factors that limit spine formation. Here, we show that SESTD1, a phospholipid-binding protein containing a lipid-binding SEC14-like domain and two spectrin-repeat cytoskeleton interaction domains, negatively regulates dendritic spine density in cultured hippocampal neurons. Overexpression of SESTD1 decreases dendritic spine density in neurons by interfering with the interaction between Rac1 and its guanine nucleotide exchange factor (GEF) Trio8. Conversely, knockdown of SESTD1 increases dendritic spine density. Further analysis reveals that the SPEC1 domain-mediated interaction with Rac1 is required for SESTD1 activity toward a decrease in dendritic spine density. Transfection of GEF domain of Trio8 into neurons rescues SESTD1-mediated decrease in dendritic spine density. More importantly, overexpression of SESTD1 results in a decrease in the frequency of miniature excitatory postsynaptic currents (mEPSCs), whereas SESTD1 knockdown increases the mEPSC frequency. These results suggest that SESTD1 may act as a negative regulator of the Rac1-Trio8 signaling pathway to reduce dendritic spine density and lower excitatory synaptic transmission in hippocampal neurons.

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“…VEGF was identified to mediate the antidepressant effect of the cAMP cascade in the adult rat hippocampus (45), and that short-term exposure of mice to an enriched environment (a large cage supplied with plastic tubes, ropes, two running wheels, and toys) produced antidepressant-like effects via a VEGF-mediated increase in spinogenesis (46). Furthermore, intracerebroventricular VEGF infusions had an antidepressant effect in behavioral models in rodents (18).…”

Section: Discussionmentioning

confidence: 98%

Alterations in VEGF expression induced by antidepressant drugs in female rats under chronic social stress

Nowacka-Chmielewska

Paul-Samojedny

Bielecka-Wajdman

et al. 2017

Experimental and Therapeutic Medicine

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Vascular endothelial growth factor (VEGF) is thought to serve a role in neurogenesis and the stress response. Although a definite link between the action of antidepressants and VEGF has not been identified, it is assumed that VEGF, as a neurotrophic factor, serves an important role in the effects of antidepressant treatment. To examine this, the present study subjected adult female rats to four weeks of social instability stress and measured the effect of antidepressant treatment on the expression of VEGF. Firstly, endocrine markers of stress and body weight were measured in parallel with behavioral tests prior to and following subjection to stress. Then, the effect of 28-day daily treatment with desipramine (DMI; 10 mg/kg), fluoxetine (5 mg/kg) or tianeptine (10 mg/kg) on the number of copies of VEGF mRNA in the amygdala, hippocampus and hypothalamus, and on serum VEGF protein levels, of rats subjected to chronic stress was determined. In addition, the weight of the adrenal glands was measured following subjection to stress. Exposure to chronic stress was found to increase the rats' sucrose preference, and diminish their tendency for general exploration and time spent in the open. The relative adrenal weights of the stressed rats were significantly increased compared with the control. Plasma concentrations of corticosterone and adrenocorticotropic hormone were not significantly augmented. In addition, the present study identified that stress elevated VEGF mRNA expression in all studied neural structures. Furthermore, the results identified that the stress-induced increase in VEGF mRNA expression in the amygdala and hypothalamus was attenuated by long-term administration of DMI. Conversely, a decrease in serum VEGF concentration was observed in stressed rats, which was not reversed by treatment with antidepressants. In conclusion, the current study suggests that under conditions of stress, VEGF serves a role in the mechanism of action of DMI, through modulating activity of the norepinephrine system.

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Vascular Endothelial Growth Factor-dependent Spinogenesis Underlies Antidepressant-like Effects of Enriched Environment

Cited by 29 publications

References 87 publications

MicroRNA-107 prevents amyloid-β-induced neurotoxicity and memory impairment in mice

MicroRNA-107 prevents amyloid-β-induced neurotoxicity and memory impairment in mice

The phospholipid-binding protein SESTD1 negatively regulates dendritic spine density by interfering with Rac1-Trio8 signaling pathway

Alterations in VEGF expression induced by antidepressant drugs in female rats under chronic social stress

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