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Signalling Networks Regulating Cell Survival and Dynamics in Brain Development and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 22133

Special Issue Editor

Prof. Dr. Jee-Yin Ahn

E-Mail Website
Guest Editor
Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 16419, Republic of Korea
Interests: cell survival; cell death; morphogenesis; synapse formation; epigenetic and transcriptional control; protein modifications; mitochondrial dysfunction; brain development; brain disease

Special Issue Information

Dear Colleagues,

Cellular signalling networks control cell survival and dynamics, which is a fundamental biological process that governs the assembly and function of neural circuits in the developing brain. Studies over the past several decades have explored the functions and consequences of the regulation of cellular signalling, including epigenetic and transcriptional control, protein modifications, and mitochondrial dysfunction, and elucidated how these mechanisms are deregulated in neurological disorders. Neurons communicate with other cells by relaying signals along axons and forming a synapse, a bridge that links neurons to its surrounding partners. Thus, discovering the regulatory signalling that contributes to neural survival and governs the morphogenesis of axons and dendrites and synapse formation/refinement in a mammalian brain will establish a field of cell-intrinsic or extrinsic regulation of neuronal connectivity and possibly provide a strong basis for elegant therapeutic strategies to neurologic/neurodevelopmental disorders.

Prof. Jee-Yin Ahn
Guest Editor

Manuscript Submission Information

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Keywords

  • cell survival
  • cell death
  • morphogenesis
  • synapse formation
  • epigenetic and transcriptional control
  • protein modifications
  • mitochondrial dysfunction
  • brain development
  • brain disease

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Published Papers (5 papers)

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Research

14 pages, 2198 KiB  
Article
Depletion of Mitochondrial Components from Extracellular Vesicles Secreted from Astrocytes in a Mouse Model of Fragile X Syndrome
by Byung Geun Ha, Jung-Yoon Heo, Yu-Jin Jang, Tae-Shin Park, Ju-Yeon Choi, Woo Young Jang and Sung-Jin Jeong
Int. J. Mol. Sci. 2021, 22(1), 410; https://doi.org/10.3390/ijms22010410 - 2 Jan 2021
Cited by 15 | Viewed by 3667
Abstract
Mitochondrial dysfunction contributes to neurodegenerative diseases and developmental disorders such as Fragile X syndrome (FXS). The cross-talk between mitochondria and extracellular vesicles (EVs) suggests that EVs may transfer mitochondrial components as intermediators for intracellular communication under physiological and pathological conditions. In the present [...] Read more.
Mitochondrial dysfunction contributes to neurodegenerative diseases and developmental disorders such as Fragile X syndrome (FXS). The cross-talk between mitochondria and extracellular vesicles (EVs) suggests that EVs may transfer mitochondrial components as intermediators for intracellular communication under physiological and pathological conditions. In the present study, the ability of EVs to transfer mitochondrial components and their role in mitochondrial dysfunction in astrocytes were examined in the brains of Fmr1 knockout (KO) mice, a model of FXS. The amounts of mitochondrial transcription factor NRF-1, ATP synthases ATP5A and ATPB, and the mitochondrial membrane protein VDAC1 in EVs were reduced in cerebral cortex samples and astrocytes from Fmr1 KO mice. These reductions correspond to decreased mitochondrial biogenesis and transcriptional activities in Fmr1 KO brain, along with decreased mitochondrial membrane potential (MMP) with abnormal localization of vimentin intermediate filament (VIF) in Fmr1 KO astrocytes. Our results suggest that mitochondrial dysfunction in astrocytes is associated with the pathogenesis of FXS and can be monitored by depletion of components in EVs. These findings may improve the ability to diagnose developmental diseases associated with mitochondrial dysfunction, such as FXS and autism spectrum disorders (ASD). Full article
(This article belongs to the Special Issue Signalling Networks Regulating Cell Survival and Dynamics in Brain Development and Disease)
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16 pages, 3507 KiB  
Article
The Molecular Floodgates of Stress-Induced Senescence Reveal Translation, Signalling and Protein Activity Central to the Post-Mortem Proteome
by Valerie C. Wasinger, Darren Curnoe, Ceridwen Boel, Naomi Machin and Hsiao Mei Goh
Int. J. Mol. Sci. 2020, 21(17), 6422; https://doi.org/10.3390/ijms21176422 - 3 Sep 2020
Cited by 4 | Viewed by 3502
Abstract
The transitioning of cells during the systemic demise of an organism is poorly understood. Here, we present evidence that organismal death is accompanied by a common and sequential molecular flood of stress-induced events that propagate the senescence phenotype, and this phenotype is preserved [...] Read more.
The transitioning of cells during the systemic demise of an organism is poorly understood. Here, we present evidence that organismal death is accompanied by a common and sequential molecular flood of stress-induced events that propagate the senescence phenotype, and this phenotype is preserved in the proteome after death. We demonstrate activation of “death” pathways involvement in diseases of ageing, with biochemical mechanisms mapping onto neurological damage, embryonic development, the inflammatory response, cardiac disease and ultimately cancer with increased significance. There is sufficient bioavailability of the building blocks required to support the continued translation, energy, and functional catalytic activity of proteins. Significant abundance changes occur in 1258 proteins across 1 to 720 h post-mortem of the 12-week-old mouse mandible. Protein abundance increases concord with enzyme activity, while mitochondrial dysfunction is evident with metabolic reprogramming. This study reveals differences in protein abundances which are akin to states of stress-induced premature senescence (SIPS). The control of these pathways is significant for a large number of biological scenarios. Understanding how these pathways function during the process of cellular death holds promise in generating novel solutions capable of overcoming disease complications, maintaining organ transplant viability and could influence the findings of proteomics through “deep-time” of individuals with no historically recorded cause of death. Full article
(This article belongs to the Special Issue Signalling Networks Regulating Cell Survival and Dynamics in Brain Development and Disease)
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20 pages, 4433 KiB  
Article
Dysregulation of Epigenetic Control Contributes to Schizophrenia-Like Behavior in Ebp1+/− Mice
by Inwoo Hwang and Jee-Yin Ahn
Int. J. Mol. Sci. 2020, 21(7), 2609; https://doi.org/10.3390/ijms21072609 - 9 Apr 2020
Cited by 3 | Viewed by 3511
Abstract
Dysregulation of epigenetic machinery can cause a variety of neurological disorders associated with cognitive abnormalities. In the hippocampus of postmortem Schizophrenia (SZ) patients, the most notable finding is the deregulation of GAD67 along with differential regulation of epigenetic factors associated with glutamate decarboxylase [...] Read more.
Dysregulation of epigenetic machinery can cause a variety of neurological disorders associated with cognitive abnormalities. In the hippocampus of postmortem Schizophrenia (SZ) patients, the most notable finding is the deregulation of GAD67 along with differential regulation of epigenetic factors associated with glutamate decarboxylase 67 (GAD67) expression. As we previously reported, ErbB3-binding protein 1 (EBP1) is a potent epigenetic regulator. EBP1 can induce repression of Dnmt1, a well-studied transcriptional repressor of GAD67. In this study, we investigated whether EBP1 contributes to the regulation of GAD67 expression in the hippocampus, controlling epigenetic machinery. In accordance with SZ-like behaviors in Ebp1(+/−) mice, heterozygous deletion of EBP1 led to a dramatic reduction of GAD67 expression, reflecting an abnormally high level of Dnmt1. Moreover, we found that EBP1 binds to the promoter region of HDAC1, which leads to histone deacetylation of GAD67, and suppresses histone deacetylase 1 (HDAC1) expression, inversely mirroring an unusually high level of HDAC1 in Ebp1(+/−) mice. However, EBP1 mutant (p.Glu 183 Ter) found in SZ patients did not elevate the expression of GAD67, failing to suppress Dnmt1 and/or HDAC1 expression. Therefore, this data supports the hypothesis that a reduced amount of EBP1 may contribute to an etiology of SZ due to a loss of transcriptional inhibition of epigenetic repressors, leading to a decreased expression of GAD67. Full article
(This article belongs to the Special Issue Signalling Networks Regulating Cell Survival and Dynamics in Brain Development and Disease)
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15 pages, 4190 KiB  
Article
A Role of Microtubules in Oligodendrocyte Differentiation
by Bo Yoon Lee and Eun-Mi Hur
Int. J. Mol. Sci. 2020, 21(3), 1062; https://doi.org/10.3390/ijms21031062 - 5 Feb 2020
Cited by 19 | Viewed by 5876
Abstract
Oligodendrocytes are specialized cells that myelinate axons in the central nervous system. Defects in oligodendrocyte function and failure to form or maintain myelin sheaths can cause a number of neurological disorders. Oligodendrocytes are differentiated from oligodendrocyte progenitor cells (OPCs), which extend several processes [...] Read more.
Oligodendrocytes are specialized cells that myelinate axons in the central nervous system. Defects in oligodendrocyte function and failure to form or maintain myelin sheaths can cause a number of neurological disorders. Oligodendrocytes are differentiated from oligodendrocyte progenitor cells (OPCs), which extend several processes that contact, elaborate, and eventually wrap axonal segments to form multilayered myelin sheaths. These processes require extensive changes in the cytoarchitecture and must be regulated by reorganization of the cytoskeleton. Here, we established a simple protocol to isolate and differentiate mouse OPCs, and by using this method, we investigated a role of microtubules (MTs) in oligodendrocyte differentiation. Oligodendrocytes developed a complex network of MTs during differentiation, and treatment of differentiating oligodendrocytes with nanomolar concentrations of MT-targeting agents (MTAs) markedly affected oligodendrocyte survival and differentiation. We found that acute exposure to vincristine and nocodazole at early stages of oligodendrocyte differentiation markedly increased MT arborization and enhanced differentiation, whereas taxol and epothilone B treatment produced opposing outcomes. Furthermore, treatment of myelinating co-cultures of oligodendrocytes and neurons with nanomolar concentrations of MTAs at late stages of oligodendrocyte differentiation induced dysmyelination. Together, these results suggest that MTs play an important role in the survival, differentiation, and myelination of oligodendrocytes. Full article
(This article belongs to the Special Issue Signalling Networks Regulating Cell Survival and Dynamics in Brain Development and Disease)
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17 pages, 2941 KiB  
Article
High Fat Diet Suppresses Peroxisome Proliferator-Activated Receptors and Reduces Dopaminergic Neurons in the Substantia Nigra
by Yu-Chia Kao, Wei-Yen Wei, Kuen-Jer Tsai and Liang-Chao Wang
Int. J. Mol. Sci. 2020, 21(1), 207; https://doi.org/10.3390/ijms21010207 - 27 Dec 2019
Cited by 35 | Viewed by 5029
Abstract
Although several epidemiologic and animal studies have revealed correlations between obesity and neurodegenerative disorders, such as Parkinson disease (PD), the underlying pathological mechanisms of obesity-induced PD remain unclear. Our study aimed to assess the effect of diet-induced obesity on the brain dopaminergic pathway. [...] Read more.
Although several epidemiologic and animal studies have revealed correlations between obesity and neurodegenerative disorders, such as Parkinson disease (PD), the underlying pathological mechanisms of obesity-induced PD remain unclear. Our study aimed to assess the effect of diet-induced obesity on the brain dopaminergic pathway. For five months, starting from weaning, we gave C57BL/6 mice a high-fat diet (HFD) to generate an obese mouse model and investigate whether the diet reprogrammed the midbrain dopaminergic system. Tyrosine hydroxylase staining showed that the HFD resulted in fewer dopaminergic neurons in the substantia nigra (SN), but not the striatum. It also induced neuroinflammation, with increased astrogliosis in the SN and striatum. Dendritic spine density in the SN of HFD-exposed mice decreased, which suggested that prolonged HFD altered dopaminergic neuroplasticity. All three peroxisome proliferator-activated receptor (PPAR) subtype (PPAR-α, PPAR-β/δ, PPAR-γ) levels were significantly reduced in the SN and the ventral tegmental area of HFD mice when compared to those in controls. This study showed that a prolonged HFD induced neuroinflammation, suppressed PPAR levels, caused degeneration of midbrain dopaminergic neurons, and resulted in symptoms reminiscent of human PD. To our knowledge, this is the first study documenting the effects of an HFD on PPARs in dopaminergic neurons. Full article
(This article belongs to the Special Issue Signalling Networks Regulating Cell Survival and Dynamics in Brain Development and Disease)
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