Depression- and anxiety-like behaviour is related to BDNF/TrkB signalling in a mouse model of psoriasis

JiaWen, W.; Sun, Hong; ShengXiang, X.; Jing, Lei

doi:10.1111/ced.13378

Cited by 30 publications

(25 citation statements)

References 19 publications

(36 reference statements)

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“…Our data showed that these DEGs were mainly enriched in the neurotrophin signaling pathway, insulin signaling pathway, alcoholism, GABAergic synapse, glutamatergic synapse, amphetamine addiction, MAPK signaling pathway, PI3K‐Akt signaling pathway and circadian rhythm (Table ). Interestingly, these signaling pathways are involved in the pathophysiology and treatment of depression . For example, GABA and glutamate neurotransmitter deficits are used to explain the neurobiological abnormalities associated with MDD, which has been well‐accepted .…”

Section: Discussionmentioning

confidence: 99%

Antidepressant mechanism of classical herbal formula lily bulb and Rehmannia decoction: insights from gene expression profile of medial prefrontal cortex of mice with stress‐induced depression‐like behavior

Zhang

Chi

Pan

et al. 2020

Genes Brain and Behavior

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According to traditional Chinese medicine, lily bulb and Rehmannia decoction (LBRD) is a specialized formula for the treatment of "lily disease", the symptoms of which resemble the clinical manifestations of major depression. However, the molecular basis of the antidepressant mechanism of LBRD and the quality marker ingredients of LBRD remain unclear. This study aimed to investigate the quality marker ingredients of LBRD and to show the molecular mechanism of its antidepressant activities. In this study, we adopted the chronic unpredicted mild stress paradigm to construct a depression model. High-performance liquid chromatography (HPLC) was used to determine the levels of the main markers in LBRD. The underlying mechanism of LBRD was explored by measuring neurotransmitter and cytokine levels using enzyme-linked immunosorbent assay, and by quantifying differentially expressed gene (DEG) of transcriptome in the medial prefrontal cortex (mPFC) tissue through RNA sequencing. HPLC results showed that the average levels of quality marker ingredients of LBRD (ferulic acid, dioscin, verbascoside and catalpol) were 0.00079%, 0.00039%, 0.7% and 1.6% (w/w), respectively. LBRD intervention significantly attenuated the depressive phenotype compared with that in the depressed group. LBRD treatment altered the enriched DEGs in the signaling pathways of γ-aminobutyric acid (GABA) and glutamate neurotransmitter, synaptic plasticity and axon guidance, circadian rhythm and neural-immunity. GABAergic and glutamatergic synapses as well as brain-derived neurotrophic factor (BDNF)/TrkB-dependent phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin-1 (mTOR1), might be the main

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Section: Discussionmentioning

confidence: 99%

Antidepressant mechanism of classical herbal formula lily bulb and Rehmannia decoction: insights from gene expression profile of medial prefrontal cortex of mice with stress‐induced depression‐like behavior

Zhang

Chi

Pan

et al. 2020

Genes Brain and Behavior

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“…Several studies have shown that fluoxetine improves BDNF expression and concentration (35)(36)(37). Some studies have shown that BDNF expression induced by fluoxetine is associated with BDNF-TRKB signalling (38,39).…”

Section: Discussionmentioning

confidence: 99%

Differential Expression of BDNF and BIM in Streptozotocin-induced Diabetic Rat Retina After Fluoxetine Injection

Kim

Chung

Hwang

et al. 2021

In Vivo

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Background: Chronic diabetic retinopathy (DR) is a diabetic complication that causes blindness. Brainderived neurotrophic factor (BDNF) expression is induced by fluoxetine. We observed the effects of fluoxetine on a streptozotocin (STZ)-induced diabetic rat model in this study. Materials and Methods: Rats were divided into three groups: Control, diabetic (65 mg/kg STZ injection), and diabetic with fluoxetine injection (20 mg/kg/week, six times). Western blotting was performed using anti-BDNF and anti-hexaribonucleotide-binding protein-3. Expression of BCL2 apoptosis regulator-like protein 11 (BIM) was analysed using a reverse transcription-polymerase chain reaction. Results: BDNF levels were significantly higher in the diabetic group treated with fluoxetine than in the untreated diabetic group. BIM expression was higher in the diabetic group than in the control group. BIM gene expression was lower in fluoxetinetreated diabetic group than in the untreated diabetic group. Conclusion: Fluoxetine had an anti-apoptotic effect with upregulation of BDNF expression in retina of rats with STZinduced diabetes.Diabetic retinopathy (DR) is a complication of diabetes that causes blindness (1). Important mechanisms of blindness are macular edema and alteration of neovascularisation (2, 3). Vascular endothelial growth factor (VEGF) is the most effective mediator of DR progression (4). Anti-VEGF effects are associated with the regression of retinal neovascularisation (5) and anti-VEGF treatment is the most effective approach for DR therapy. However, some patients show poor response to this treatment (6). Thus, comprehension of the pathogenesis of DR is critical. Although DR is traditionally known as a vascular disease, some studies have shown that neuronal pathological changes occur in the retina, including physiological and structural alterations (7, 8).Brain-derived neurotrophic factor (BDNF) is a neuroprotective growth factor that affects neuronal cell proliferation and survival (9). BDNF binds to tropomyosin receptor kinase B (TRKB), which leads to nerve cell survival, repair, and development through the neurotrophic signalling pathway (10). BDNF has also been observed in retinal neuronal cells. BDNF is expressed in retinal ganglion cells (RGCs) and was found to play an important role in their survival in rats with streptozotocin (STZ)-induced diabetes (11). Cusato et al. reported that BDNF prevented cell death in the inner nuclear layer of the retina (12). Uzel et al. showed that BDNF is a good marker for the early diagnosis of DR (13).In a previous study, BDNF expression was induced by fluoxetine, a selective inhibitor of serotonin reuptake, to treat major depression (14). In this study, we analysed the expression of BDNF and BCL2 apoptosis regulator-like protein 11 (BIM) after fluoxetine injection in the STZinduced diabetes rat model to investigate the effect of fluoxetine on BDNF signalling. Materials and MethodsRat model of DR. All animal studies were approved by the Chosun University Institutional Animal Care and Use C...

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“…Th17 cells may have a significant role in depression, while high levels of IL17 and IL17A high levels could be involved in psoriasis-associated depression [15,16,17] . In a mouse psoriasis model, the antidepression and anti-anxiety drug-fluoxetine, significantly contributed to improvement [18] .…”

Section: Introductionmentioning

confidence: 99%

Optimization of psoriasis mouse models

Karamani

Antoniadou

Dimou

et al. 2021

Journal of Pharmacological and Toxicological Methods

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Psoriasis, a common chronic, autoimmune, inflammatory, relapsing disease should benefit from reliable and human relevant animal models in order to pre-clinically test drugs and approach their mechanism of action. Due to ease of use, convenience and low cost, imiquimod (IMQ) induced psoriasis-like model is widely utilized; however, are all mouse strains equivalent, is the hairless mouse utilizable and can the imiquimod model be further optimized? Under similar experimental conditions, common mouse strains (BALB/c, C57BL/6J, ApoE) and a new hairless strain (ApoE/SKH-hr2) as well as several inducers (IMQ, IMQ + Acetic Acid (AcOH) topical and IMQ +AcOH systemic) were compared by clinical, histopathological, biophysical and locomotor activity assessment. Results showed that BALB/c mice yielded optimal psoriasislike phenotype with IMQ+AcOH topical treatment, C57BL/6J moderate, ApoE mild, while the ApoE/SKH-hr2 mice due to Munro abscess absence in histopathology analysis left doubts about the psoriasis-like acquisition. The locomotor activity of BALB/c mice treated with IMQ, IMQ+AcOH topically and IMQ+AcOH systemically, showed with all treatments, a decreased covered distance and rearing and an increased immobility. In conclusion, BALB/c appears an optimal psoriasis-like model when utilizing IMQ+AcOH topical application.

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Depression- and anxiety-like behaviour is related to BDNF/TrkB signalling in a mouse model of psoriasis

Abstract: BDNF/TrkB signalling participates in the pathological mechanism of depression and anxiety behaviours in psoriasis. Our findings provide a new therapeutic strategy for the treatment of skin lesions in psoriasis.

Cited by 30 publications

References 19 publications

Antidepressant mechanism of classical herbal formula lily bulb and Rehmannia decoction: insights from gene expression profile of medial prefrontal cortex of mice with stress‐induced depression‐like behavior

Antidepressant mechanism of classical herbal formula lily bulb and Rehmannia decoction: insights from gene expression profile of medial prefrontal cortex of mice with stress‐induced depression‐like behavior

Differential Expression of BDNF and BIM in Streptozotocin-induced Diabetic Rat Retina After Fluoxetine Injection

Optimization of psoriasis mouse models

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