Neuronal Excitability in Epileptogenic Zones Regulated by the Wnt/ Β-Catenin Pathway

Rubio, Carmen; Taddei, Elisa; Acosta, José Ángel; Custodio, Verónica; Paz, Carlos

doi:10.2174/1871527319666200120143133

Cited by 10 publications

(5 citation statements)

References 96 publications

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“…SFRP1 participates in the regulation of WNT/β-catenin pathway by suppressing the accumulation of β-catenin through a GSK-3 dependent mechanism, which interferes with the binding receptor of WNT and FRIZZLED protein (Kawano & Kypta 2003;Galli et al, 2006). The WNT/β-catenin pathway regulates hippocampal neurogenesis, synaptic division, and mitochondrial regulation, and is critical to the development and function of the central nervous system (Rubio et al, 2020). WNT/β-catenin signals modulate epileptic neurogenesis and neuronal death.…”

Section: Discussionmentioning

confidence: 99%

LncRNA UCA1 alleviates aberrant hippocampal neurogenesis through regulating miR-375/SFRP1-mediated WNT/β-catenin pathway in kainic acid-induced epilepsy

Diao

et al. 2021

Acta Biochim Pol

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Temporal lobe epilepsy (TLE) is a chronic disease of the nervous system, associated with increased proliferation in the hippocampus. Urothcarcinoma associated 1 (UCA1) is a long long non-coding RNA that was shown to regulate proliferation and differentiation of neural progenitors in vitro. We hypothesised that TLE-associated abnormal proliferation is a consequence of the downregulation of UCA1. This hypothesis was tested in mice with kainic acid (KA)-induced seizures, and then the potential mechanism was explored in vitro and in vivo. Result showed that the expression of UCA1 and Secreted Frizzled Related Protein 1 (SFRP1) were significantly reduced in hippocampal tissues of epileptic mice, while miR-375 was increased compared with the control group. Pearson correlation analysis showed that UCA1 was positively correlated with SFRP1, while miR-375 was negatively correlated with UCA1 and SFRP1. Besides, UCA1 was overexpressed in mice and the overexpression of UCA1 significantly reversed the abnormal proliferation of hippocampal neurons in epilepsy mice. In vitro Luciferase assay showed that UCA1 and Sfrp1 are both the targets of miR-375, and UCA1 promotes the expression of Sfrp1 by competitively adsorbing miR-375, thereby inhibiting the activation of the WNT/β-catenin pathway. The inactivation of the WNT/β-catenin pathway prevented the abnormal proliferation of neural progenitors in the epileptic hippocampus. In conclusion, our findings provide a theoretical basis for the clinical application of UCA1.

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Section: Discussionmentioning

confidence: 99%

LncRNA UCA1 alleviates aberrant hippocampal neurogenesis through regulating miR-375/SFRP1-mediated WNT/β-catenin pathway in kainic acid-induced epilepsy

Diao

et al. 2021

Acta Biochim Pol

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“…SETD1A has been proposed to regulate neuronal progenitor proliferation through its interaction with Histone Cell Cycle Regulator (HIRA) (Li and Jiao, 2017) could contribute to the regulation of neuronal differentiation and excitability by transcriptionally activating β-catenin (Li and Jiao, 2017), a key component of the Wnt/β-catenin pathway which is essential for neurogenesis (Hirabayashi et al, 2004;Zhang et al, 2011;Rubio et al, 2020). In mice, a missense mutation in SETD1A resulted in faster migration of neurons within the cortex (Yu X. et al, 2019), suggesting that neuronal migration could also be regulated by SETD1A.…”

Section: Mll4/kmt2d In Kabuki Syndrome Associated With Microcephalymentioning

confidence: 99%

The role of histone methyltransferases in neurocognitive disorders associated with brain size abnormalities

Ritchie

Lizarraga

2023

Front. Neurosci.

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Brain size is controlled by several factors during neuronal development, including neural progenitor proliferation, neuronal arborization, gliogenesis, cell death, and synaptogenesis. Multiple neurodevelopmental disorders have co-morbid brain size abnormalities, such as microcephaly and macrocephaly. Mutations in histone methyltransferases that modify histone H3 on Lysine 36 and Lysine 4 (H3K36 and H3K4) have been identified in neurodevelopmental disorders involving both microcephaly and macrocephaly. H3K36 and H3K4 methylation are both associated with transcriptional activation and are proposed to sterically hinder the repressive activity of the Polycomb Repressor Complex 2 (PRC2). During neuronal development, tri-methylation of H3K27 (H3K27me3) by PRC2 leads to genome wide transcriptional repression of genes that regulate cell fate transitions and neuronal arborization. Here we provide a review of neurodevelopmental processes and disorders associated with H3K36 and H3K4 histone methyltransferases, with emphasis on processes that contribute to brain size abnormalities. Additionally, we discuss how the counteracting activities of H3K36 and H3K4 modifying enzymes vs. PRC2 could contribute to brain size abnormalities which is an underexplored mechanism in relation to brain size control.

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“…Neurons receive electrochemical signals from other neurons through dendrites, which then communicate information to target cells through the soma and along the axon [40]. Furthermore, neurons are also "excitable" cells, which produce different oscillatory activities that help to understand the transmitting and processing of signals in neural system [41]. The neuronal surface membrane contains ion channels that allow small charged atoms to pass.…”

Section: Neuron Cellmentioning

confidence: 99%

The Neuroprotection Effects of Exosome in Central Nervous System Injuries: a New Target for Therapeutic Intervention

2022

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Central nervous system (CNS) injuries, including traumatic brain injury (TBI), spinal cord injury (SCI) and subarachnoid hemorrhage (SAH), are the most common cause of death and disability around the world. As a key subset of extracellular vesicles (EVs), exosomes have recently attracted great attentions due to their functions in remodeling extracellular matrix, and transmitting signals and molecules. A large number of studies have suggested that exosomes played an important role in brain development and involved in many neurological disorders, particularly in CNS injuries. It has been proposed that exosomes could improve cognition function, inhibit apoptosis, suppress in ammation, regulate autophagy and protect blood brain barrier (BBB) in CNS injuries via different molecules and pathways including microRNA (miRNA), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), ph1osphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B (PI3K/AKT), Notch1 and extracellular regulated protein kinases (ERK). Therefore, exosomes showed great promise as potential targets in CNS injuries. In this article, we present a review highlighting the applications of exosomes in CNS injuries. Hence, on the basis of these properties and effects, exosomes may be developed as therapeutic agents for CNS injury patients.

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Neuronal Excitability in Epileptogenic Zones Regulated by the Wnt/ Β-Catenin Pathway

Cited by 10 publications

References 96 publications

LncRNA UCA1 alleviates aberrant hippocampal neurogenesis through regulating miR-375/SFRP1-mediated WNT/β-catenin pathway in kainic acid-induced epilepsy

LncRNA UCA1 alleviates aberrant hippocampal neurogenesis through regulating miR-375/SFRP1-mediated WNT/β-catenin pathway in kainic acid-induced epilepsy

The role of histone methyltransferases in neurocognitive disorders associated with brain size abnormalities

The Neuroprotection Effects of Exosome in Central Nervous System Injuries: a New Target for Therapeutic Intervention

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