Role of miR-124 in the regulation of retinoic acid-induced Neuro-2A cell differentiation

You, Qun; Gong, Qiang; Han, Yuqiao; Pi, Rou; Du, Yanqiu; Shen, Dong

doi:10.4103/1673-5374.270417

Cited by 11 publications

(4 citation statements)

References 52 publications

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“…For example, the inhibitor of miR-128 upregulated the expression of PPAR-γ to reduce Aβ-mediated cytotoxicity via inactivation of NF-κB in N2a cells (26). Others have shown that miR-124 encourages mouse neuroblastoma N2a cells to differentiate toward a neuronal phenotype (27)(28)(29). In this work, we hypothesized that miR-669b-5p was associated with CHEK2 in Neuro2a APPSwe/Δ9 cells using bioinformatics.…”

Section: Discussionmentioning

confidence: 98%

MiR-669b-5p inhibits the Alzheimer's disease development via regulation of CHEK2 in Neuro2a APPSwe/Δ9 cells

Mula A,

Yan Bai,

Bingcheng Hu

et al. 2023

Cell Mol Biol (Noisy-le-grand)

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Section: Discussionmentioning

confidence: 98%

MiR-669b-5p inhibits the Alzheimer's disease development via regulation of CHEK2 in Neuro2a APPSwe/Δ9 cells

Mula A,

Yan Bai,

Bingcheng Hu

et al. 2023

Cell Mol Biol (Noisy-le-grand)

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“…In addition, the same trend of increasing TUJ1+ cells as seen in neurospheres was observed, suggesting that infection may lead to interruption (or, at least, a delay) in TUJ1 to NF-200 progression. Neurite outgrowth has been evaluated in Neuro2a cells by other groups under different stimuli/treatments, and it has been reported that this process can be modulated by carbazole derivatives (Furukawa et al, 2019), miRNA (You et al, 2020), Mob proteins (Lin et al, 2011) and polyphenols, including Resveratrol and Apigenin (Namsi et al, 2018). Interestingly, Resveratrol has been shown to revert T. gondii -induced cytokine release and purinergic signaling imbalance in neural progenitor cells (Bottari et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Infection of mouse neural progenitor cells by Toxoplasma gondii affects in vitro proliferation, differentiation and migration

Pires

Barbosa

Santiago

et al. 2021

Preprint

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Congenital toxoplasmosis constitutes a major cause of pre- and post-natal complications. Fetal infection with Toxoplasma gondii influences development and can lead to microcephaly, encephalitis, and neurological abnormalities. Few studies have attempted to explain the impact of T. gondii infection on the physiology of mature nerve cells, and no systematic study concerning the effect of infection of neural progenitor cells by T. gondii in the biology of these progenitors is available. We infected cortical intermediate progenitor cell cultivated as neurospheres obtained from E16.5 Swiss Webster mice with T. gondii (Me49 strain) tachyzoites to mimic the developing mouse cerebral cortex in vitro. Infection decreased cell proliferation as detected by Ki67 staining at 48 and 72 hours post infection (hpi) in floating neurospheres, resulting in reduced cellularity at 96 hpi. Neurogenic and gliogenic potential, assessed in plated neurospheres, was shown to be impaired in infected cultures, as indicated by neurofilament heavy chain (NF-200) and GFAP staining, respectively. To further investigate the impact of infection on neuronal differentiation, Neuro2a neuroblasts were infected and after 24 hpi, neurogenic differentiation was induced with serum withdrawal. We confirmed that infection induces a decrease in neuroblast-neuron differentiation rates in cells stained for NF-200, with reduced neuritogenesis. Migration rates were analyzed in plated neurospheres. At 120 h after plating, infected cultures exhibited decreased overall migration rates and altered the radial migration of nestin-, GFAP- and NF-200-positive cells. These findings indicate that T. gondii infection of neural progenitor cells may lead to reduced neuro/gliogenesis due to an imbalance in cell proliferation alongside an altered migratory profile. If translated to the in vivo situation, these data could explain, in part, the cortical malformations observed in congenitally infected individuals.

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“…The vertebrate brain has a high expression of miRNAs, highlighting the importance of post-transcriptional regulation in nervous system function (Miska et al, 2004 ; Sempere et al, 2004 ; Lau and Hudson, 2010 ). MiRNA expression profiles have now identified specific miRNAs important for various RA-induced processes (reviewed in Gholikhani-Darbroud, 2020 ; Wang et al, 2020 ), including neuronal differentiation (Le et al, 2009 ; Annibali et al, 2012 ; Hu et al, 2017 ; Gao et al, 2019 ; You et al, 2020 ), axonal outgrowth (Su et al, 2020 ), and CNS organization (Qin et al, 2016 ; Liu et al, 2020 ).…”

Section: Development: a Brief Overview Of The Role Of Retinoidsmentioning

confidence: 99%

Non-canonical retinoid signaling in neural development, regeneration and synaptic function

Piazza,

Carlone,

Spencer

2024

Front. Mol. Neurosci.

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Canonical retinoid signaling via nuclear receptors and gene regulation is critical for the initiation of developmental processes such as cellular differentiation, patterning and neurite outgrowth, but also mediates nerve regeneration and synaptic functions in adult nervous systems. In addition to canonical transcriptional regulation, retinoids also exert rapid effects, and there are now multiple lines of evidence supporting non-canonical retinoid actions outside of the nucleus, including in dendrites and axons. Together, canonical and non-canonical retinoid signaling provide the precise temporal and spatial control necessary to achieve the fine cellular coordination required for proper nervous system function. Here, we examine and discuss the evidence supporting non-canonical actions of retinoids in neural development and regeneration as well as synaptic function, including a review of the proposed molecular mechanisms involved.

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Role of miR-124 in the regulation of retinoic acid-induced Neuro-2A cell differentiation

Cited by 11 publications

References 52 publications

MiR-669b-5p inhibits the Alzheimer's disease development via regulation of CHEK2 in Neuro2a APPSwe/Δ9 cells

MiR-669b-5p inhibits the Alzheimer's disease development via regulation of CHEK2 in Neuro2a APPSwe/Δ9 cells

Infection of mouse neural progenitor cells by Toxoplasma gondii affects in vitro proliferation, differentiation and migration

Non-canonical retinoid signaling in neural development, regeneration and synaptic function

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