Brain Beta-Catenin Signalling During Stress and Depression

Teo, Chuin Hau; Soga, Tomoko; Parhar, Ishwar S.

doi:10.1159/000487764

Cited by 35 publications

(23 citation statements)

References 84 publications

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Section: Dicer In Human Diseasesmentioning

confidence: 99%

“…Chronic stress, a condition commonly associated with depression, can cause changes in the endocrine system, as well as alterations in the expression of genes related to stress response [ 75 , 76 ]. Chronic stress is both a psychological and neurobiological phenomenon, and has been shown to alter the hypothalamo-pituitary-adrenal (HPA) system [ 75 , 77 ]. It may also affect hippocampus and prefrontal cortex volume, as well as dendritic growth in the amygdala, leading to impairment of memory and emotional control, and augmentation of anxiety and aggression, respectively [ 78 ].…”

Section: Dicer In Human Diseasesmentioning

confidence: 99%

“…It may also affect hippocampus and prefrontal cortex volume, as well as dendritic growth in the amygdala, leading to impairment of memory and emotional control, and augmentation of anxiety and aggression, respectively [ 78 ]. During stress and depression, many biological processes and components undergo changes, with the serotonergic system, the Wnt signaling pathway and β-catenin expression being typical examples [ 75 ]. β-catenin, a fundamental component of the canonical Wnt signaling pathway, is a ubiquitously expressed protein in the mammalian brain that is involved in both intercellular adhesion and gene transcription [ 79 , 80 ].…”

Section: Dicer In Human Diseasesmentioning

confidence: 99%

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Dicing the Disease with Dicer: The Implications of Dicer Ribonuclease in Human Pathologies

Theotoki

Pantazopoulou

Georgiou

et al. 2020

IJMS

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Gene expression dictates fundamental cellular processes and its de-regulation leads to pathological conditions. A key contributor to the fine-tuning of gene expression is Dicer, an RNA-binding protein (RBPs) that forms complexes and affects transcription by acting at the post-transcriptional level via the targeting of mRNAs by Dicer-produced small non-coding RNAs. This review aims to present the contribution of Dicer protein in a wide spectrum of human pathological conditions, including cancer, neurological, autoimmune, reproductive and cardiovascular diseases, as well as viral infections. Germline mutations of Dicer have been linked to Dicer1 syndrome, a rare genetic disorder that predisposes to the development of both benign and malignant tumors, but the exact correlation of Dicer protein expression within the different cancer types is unclear, and there are contradictions in the data. Downregulation of Dicer is related to Geographic atrophy (GA), a severe eye-disease that is a leading cause of blindness in industrialized countries, as well as to psychiatric and neurological diseases such as depression and Parkinson’s disease, respectively. Both loss and upregulation of Dicer protein expression is implicated in severe autoimmune disorders, including psoriasis, ankylosing spondylitis, rheumatoid arthritis, multiple sclerosis and autoimmune thyroid diseases. Loss of Dicer contributes to cardiovascular diseases and causes defective germ cell differentiation and reproductive system abnormalities in both sexes. Dicer can also act as a strong antiviral with a crucial role in RNA-based antiviral immunity. In conclusion, Dicer is an essential enzyme for the maintenance of physiology due to its pivotal role in several cellular processes, and its loss or aberrant expression contributes to the development of severe human diseases. Further exploitation is required for the development of novel, more effective Dicer-based diagnostic and therapeutic strategies, with the goal of new clinical benefits and better quality of life for patients.

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Section: Dicer In Human Diseasesmentioning

confidence: 99%

Section: Dicer In Human Diseasesmentioning

confidence: 99%

Section: Dicer In Human Diseasesmentioning

confidence: 99%

See 1 more Smart Citation

Dicing the Disease with Dicer: The Implications of Dicer Ribonuclease in Human Pathologies

Theotoki

Pantazopoulou

Georgiou

et al. 2020

IJMS

View full text Add to dashboard Cite

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“…In general, increased corticosteroids, due to stress and depression, interfere with β-catenin in the nervous system [54]. Furthermore, stress induces expression of soluble Wnt antagonists that interfere with β-catenin expression, and induces neuronal death [51,55].…”

Section: Plos Onementioning

confidence: 99%

Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle

et al. 2020

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When herpes simplex virus 1 (HSV-1) infection is initiated in the ocular, nasal, or oral cavity, sensory neurons within trigeminal ganglia (TG) become infected. Following a burst of viral transcription in TG neurons, lytic cycle viral genes are suppressed and latency is established. The latency-associated transcript (LAT) is the only viral gene abundantly expressed during latency, and LAT expression is important for the latency-reactivation cycle. Reactivation from latency is required for virus transmission and recurrent disease, including encephalitis. The Wnt/β-catenin signaling pathway is differentially expressed in TG during the bovine herpesvirus 1 latency-reactivation cycle. Hence, we hypothesized HSV-1 regulates the Wnt/β-catenin pathway and promotes maintenance of latency because this pathway enhances neuronal survival and axonal repair. New studies revealed β-catenin was expressed in significantly more TG neurons during latency compared to TG from uninfected mice or mice latently infected with a LAT -/mutant virus. When TG explants were incubated with media containing dexamethasone to stimulate reactivation, significantly fewer β-cate-nin+ TG neurons were detected. Conversely, TG explants from uninfected mice or mice latently infected with a LAT -/mutant increased the number of β-catenin+ TG neurons in the presence of DEX relative to samples not treated with DEX. Impairing Wnt signaling with small molecule antagonists reduced virus shedding during explant-induced reactivation. These studies suggested β-catenin was differentially expressed during the latency-reactivation cycle, in part due to LAT expression. OPEN ACCESS Citation: Harrison KS, Zhu L, Thunuguntla P, Jones C (2020) Herpes simplex virus 1 regulates βcatenin expression in TG neurons during the latency-reactivation cycle. PLoS ONE 15(3): e0230870. https://doi.

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“…In which GSK-3β phosphorylates β-catenin and lead to its proteosomal degradation and restricts further gene transcription. In stressful condition especially in depression β-catenin expression downregulates [19, 20]. Moreover, chronic electroconvulsive therapy upregulates β-catenin expression in the hippocampus and stimulate hippocampal neurogenesis even in severe depression like drug resistant depression [19].…”

Section: Introductionmentioning

confidence: 99%

Exploring the potential role of sonic hedgehog cell signalling pathway in antidepressant effects of nicotine in chronic unpredictable mild stress rat model

Tayyab

Shahi

Farheen

et al. 2019

Heliyon

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Nicotine is the most common and highly addictive drug of abuse, associated with several life-threatening diseases and high mortality. Nicotine abuse is the concerted effort to feel reward and fight depression in depressed individuals. The underlying mechanism of nicotine is to activate the brain reward system in the central nervous system and provide an antidepressant effect. Antidepressants provide their therapeutic effect by stimulating hippocampal neurogenesis, which can be correlated with brain derived neurotrophic factor (BDNF) expression in the hippocampus. BDNF interacts with Wnt/β-catenin and sonic hedgehog (Shh) signalling cascade to stimulate hippocampal neurogenesis. Shh is the marker of hippocampal neurogenesis and also involved in the neuropathology of depression. But knowledge in this area to identify the potential therapeutic target is limited. In our study, we explored the role of BDNF, Wnt/β-catenin and Shh signalling in depression and the involvement of these signalling pathways in providing an antidepressant effect by nicotine. Our investigations showed that chronic unpredictable mild stress induced depression results declined expression of BDNF, Wnt/β-catenin, Shh and its downstream transcription factors GLI1/2/3 and NKX2.2 in the hippocampus of male Wistar rat. Moreover, we also observed that nicotine administration increased the expression of these signalling molecules in providing the antidepressant effects.

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Brain Beta-Catenin Signalling During Stress and Depression

Cited by 35 publications

References 84 publications

Dicing the Disease with Dicer: The Implications of Dicer Ribonuclease in Human Pathologies

Dicing the Disease with Dicer: The Implications of Dicer Ribonuclease in Human Pathologies

Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle

Exploring the potential role of sonic hedgehog cell signalling pathway in antidepressant effects of nicotine in chronic unpredictable mild stress rat model

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