A Brain-Region-Specific Neural Pathway Regulating Germinal Matrix Angiogenesis

Ma, Shang; Santhosh, Devi; Kumar, T. Peeyush; Huang, Zhen

doi:10.1016/j.devcel.2017.04.014

Cited by 37 publications

(39 citation statements)

References 66 publications

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“…Taken together, this study, together with recently published reports (Kask et al, ; Ma et al, ), strongly suggest that RIC8A is one of the key factors governing the development of the nervous system, and being indispensable in cortical morphogenesis, angiogenesis, and in the generation of the neural crest cell‐derived structures.…”

Section: Discussionsupporting

confidence: 83%

Targeted deletion of RIC8A in mouse neural precursor cells interferes with the development of the brain, eyes, and muscles

Kask

Tikker

Ruisu

et al. 2018

Developmental Neurobiology

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Autosomal recessive disorders such as Fukuyama congenital muscular dystrophy, Walker-Warburg syndrome, and the muscle-eye-brain disease are characterized by defects in the development of patient's brain, eyes, and skeletal muscles. These syndromes are accompanied by brain malformations like type II lissencephaly in the cerebral cortex with characteristic overmigrations of neurons through the breaches of the pial basement membrane. The signaling pathways activated by laminin receptors, dystroglycan and integrins, control the integrity of the basement membrane, and their malfunctioning may underlie the pathologies found in the rise of defects reminiscent of these syndromes. Similar defects in corticogenesis and neuromuscular disorders were found in mice when RIC8A was specifically removed from neural precursor cells. RIC8A regulates a subset of G-protein α subunits and in several model organisms, it has been reported to participate in the control of cell division, signaling, and migration. Here, we studied the role of RIC8A in the development of the brain, muscles, and eyes of the neural precursor-specific conditional Ric8a knockout mice. The absence of RIC8A severely affected the attachment and positioning of radial glial processes, Cajal-Retzius' cells, and the arachnoid trabeculae, and these mice displayed additional defects in the lens, skeletal muscles, and heart development. All the discovered defects might be linked to aberrancies in cell adhesion and migration, suggesting that RIC8A has a crucial role in the regulation of cell-extracellular matrix interactions and that its removal leads to the phenotype characteristic to type II lissencephaly-associated diseases. © 2018 Wiley Periodicals, Inc. Develop Neurobiol 78: 374-390, 2018.

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Section: Discussionsupporting

confidence: 83%

Targeted deletion of RIC8A in mouse neural precursor cells interferes with the development of the brain, eyes, and muscles

Kask

Tikker

Ruisu

et al. 2018

Developmental Neurobiology

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“…On the other hand, the gut microbiota is able to produce and modulate neurotransmitters in both CNS and peripheral nervous system, and intestinal environmental changes can affect lymphocytes of the gut to produce more cytokines and chemokines, such as interleukin 1 (IL-1), IL-6, IL-17, IL-22, tumor necrosis factor-α (TNF-α; Thaiss et al, 2016 ; Sochocka et al, 2019 ), and transforming growth factor β (Ma et al, 2017 ), as well as chemokine, fractalkine, and its receptor (CX3CR1; Merino et al, 2011 ), affecting the CNS through activating the endocrine or paracrine systems. The proinflammatory cytokines, IL-1, IL-6, IL-17, and TNF-α, are potentially harmful to the brain (Angelucci et al, 2019 ).…”

Section: Links Between Gut and Brain Via Microbiommentioning

confidence: 99%

Target Dysbiosis of Gut Microbes as a Future Therapeutic Manipulation in Alzheimer’s Disease

Zhu

Chu

et al. 2020

Front. Aging Neurosci.

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Alzheimer’s disease (AD) is commonly an age-associated dementia with neurodegeneration. The pathogenesis of AD is complex and still remains unclear. The inflammation, amyloid β (Aβ), and neurofibrillary tangles as well misfolded tau protein in the brain may contribute to the occurrence and development of AD. Compared with tau protein, Aβ is less toxic. So far, all efforts made in the treatments of AD with targeting these pathogenic factors were unsuccessful over the past decades. Recently, many studies demonstrated that changes of the intestinal environment and gut microbiota via gut–brain axis pathway can cause neurological disorders, such as AD, which may be involved in the pathogenesis of AD. Thus, remodeling the gut microbiota by various ways to maintain their balance might be a novel therapeutic strategy for AD. In the review article, we analyzed the characteristics of gut microbiota and its dysbiosis in AD and its animal models and investigated the possibility of targeting the gut microbiota in the treatment of the patients with AD in the future.

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“…Cerebral palsy (Cp) is a chronic childhood disorder that can be caused by hypoxic-ischemic (HI) injury, germinal matrix hemorrhage, extreme prematurity, etc., which leads to neural behavior disorders, learning disorders, and cognitive disorder [1][2][3]. HI injury affects 1-3 per 1000 full-term infants, and is related with high mortality of Cp [4].…”

Section: Introductionmentioning

confidence: 99%

LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF

Zhao

Jian

et al. 2018

Cell Cycle

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Objective: To investigate the underlying mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in hypoxic-ischemic (HI)-induced neonatal cerebral palsy. Materials and methods: Neonatal rat model of HI injury was established to detect the motor function. LncRNA MIAT, miR-211, glial cell line-derived neurotrophic factor (GDNF) and caspase-3 expressions were measured by qRT-PCR or western blot. The apoptosis of Neuro2A cells was detected by flow cytometry. RNA immunoprecipitation (RIP) and RNA pull-down assays were performed to confirm the interaction between MIAT and miR-211. Results: Compared with control group, lncRNA MIAT and GDNF were downregulated in striatal tissues of neonatal rats in HI group and oxygen glucose deprivation (OGD)-induced ischemic injury of Neuro2A cells, whereas miR-211 was up-regulated in striatal tissues of HI group and OGDinduced ischemic injury of Neuro2A cells. LncRNA MIAT interacted with miR-211, and lncRNA MIAT overexpression reduced neuron apoptosis through miR-211. Besides, GDNF expression was positively regulated by lncRNA MIAT and negatively regulated by miR-211 in Neuro2A cells. In vivo experiment proved MIAT promoted motor function and relieved HI injury. Conclusion: MIAT overexpression reduced apoptosis of Neuro2A cells through miR-211/GDNF, which relieved HI injury of neonatal rats.

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A Brain-Region-Specific Neural Pathway Regulating Germinal Matrix Angiogenesis

Cited by 37 publications

References 66 publications

Targeted deletion of RIC8A in mouse neural precursor cells interferes with the development of the brain, eyes, and muscles

Targeted deletion of RIC8A in mouse neural precursor cells interferes with the development of the brain, eyes, and muscles

Target Dysbiosis of Gut Microbes as a Future Therapeutic Manipulation in Alzheimer’s Disease

LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF

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