RETRACTED: The regulation of survival and differentiation of neural stem cells by miR-124 via modulating PAX3

Wei, Chunxia; Ren, Lanfen; Li, Kui; Lu, Zuneng

doi:10.1016/j.neulet.2018.05.051

Cited by 12 publications

(6 citation statements)

References 23 publications

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“…Kioussi et al (1995) observed a positive, rather than a negative, correlation between Pax3 mRNA levels and GFAP protein in mouse Schwann cells in vivo and in culture during development, and also in response to injury and upon microinjection of a Pax3 expression vector. Similarly, although Wei et al (2018) did observe an inverse relationship between PAX3 and GFAP during differentiation of mouse NECs, levels of both were increased in NECs following exposure to a microRNA inhibitor. A positive correlation between PAX3 and GFAP levels was also observed by Yang et al (2016) during differentiation of mouse NECs adapted to grow in low glucose.…”

Section: Pax3mentioning

confidence: 80%

Regulation of GFAP Expression

Brenner

Messing

2021

ASN Neuro

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Expression of the GFAP gene has attracted considerable attention because its onset is a marker for astrocyte development, its upregulation is a marker for reactive gliosis, and its predominance in astrocytes provides a tool for their genetic manipulation. The literature on GFAP regulation is voluminous, as almost any perturbation of development or homeostasis in the CNS will lead to changes in its expression. In this review, we limit our discussion to mechanisms proposed to regulate GFAP synthesis through a direct interaction with its gene or mRNA. Strengths and weaknesses of the supportive experimental findings are described, and suggestions made for additional studies. This review covers 15 transcription factors, DNA and histone methylation, and microRNAs. The complexity involved in regulating the expression of this intermediate filament protein suggests that GFAP function may vary among both astrocyte subtypes and other GFAP-expressing cells, as well as during development and in response to perturbations.

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Section: Pax3mentioning

confidence: 80%

Regulation of GFAP Expression

Brenner

Messing

2021

ASN Neuro

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“…Review of the top doubly significant genes and significant GO terms (i.e. neurogenesis) revealed several genes of particular interest (Table 1), five of which encode transcription factors (Tfap2b, Pax3, Zic5, Tbx3 and Nkx6-1) that control neuronal or glial cell fate [28][29][30][31][32][33][34] . Another gene, Stmn2, was downregulated in Chd7 Gt/Gt cells and encodes a stathmin protein family member that promotes neuronal growth 35 .…”

Section: Chd7 Regulates Genes Expression Chd7 Enrichment In the Genementioning

confidence: 99%

CHD7 promotes neural progenitor differentiation in embryonic stem cells via altered chromatin accessibility and nascent gene expression

Yao

Hannum

Zhai

et al. 2020

Sci Rep

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CHARGE syndrome, a rare multiple congenital anomaly condition, is caused by haploinsufficiency of the chromatin remodeling protein gene CHD7 (Chromodomain helicase DNA binding protein 7). Brain abnormalities and intellectual disability are commonly observed in individuals with CHARGE, and neuronal differentiation is reduced in CHARGE patient-derived iPSCs and conditional knockout mouse brains. However, the mechanisms of CHD7 function in nervous system development are not well understood. In this study, we asked whether CHD7 promotes gene transcription in neural progenitor cells via changes in chromatin accessibility. We used Chd7 null embryonic stem cells (ESCs) derived from Chd7 mutant mouse blastocysts as a tool to investigate roles of CHD7 in neuronal and glial differentiation. Loss of Chd7 significantly reduced neuronal and glial differentiation. Sholl analysis showed that loss of Chd7 impaired neuronal complexity and neurite length in differentiated neurons. Genome-wide studies demonstrated that loss of Chd7 leads to modified chromatin accessibility (ATAC-seq) and differential nascent expression (Bru-Seq) of neural-specific genes. These results suggest that CHD7 acts preferentially to alter chromatin accessibility of key genes during the transition of NPCs to neurons to promote differentiation. Our results form a basis for understanding the cell stage-specific roles for CHD7-mediated chromatin remodeling during cell lineage acquisition.

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“…In the presence of myogenic regulatory factors, myoblasts proliferate and accumulate in muscle tissue, and then initiate the differentiation program. Myoblasts exit the cell cycle in an irreversible manner, gradually fuse to form multinucleated myotubes, and further differentiate to form myofibers, which migrate to injured muscle tissue to achieve the self-repair of muscle fibers (47,48). The process of myoblast proliferation and fusion to form myotubes governs the development of skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

Network pharmacology-based analysis of the effects of puerarin on sarcopenia

Chen¹,

Wang²,

Liu³

et al. 2022

Ann Transl Med

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Background: With the acceleration of population aging, sarcopenia will place a heavy burden on families and society. Thus, effective treatments urgently need to be developed to slow down the development of sarcopenia. This study adopted a network pharmacological approach to explore the possible mechanisms of puerarin in treating sarcopenia. Methods:The potential therapeutic targets of puerarin were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) database, while the targets of sarcopenia were obtained from the GeneCards, DisGeNET, Online Mendelian Inheritance in Man (OMIM), and Therapeutic Target Database (TTD) databases. The protein-protein interaction (PPI) network was generated by BisoGenet, and core targets were identified by a topological analysis. To determine the potential targeting pathways, the core targets were further imported into the Metascape platform for the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. The results were visualized using an online bioinformatics tool.Results: We identified 53 targets for puerarin and 129 targets for sarcopenia. A total of 206 core targets, which were considered potential therapeutic targets, were identified from the merged PPI network. Further, the GO and KEGG analyses revealed that the functions of the core targets and related pathways were mainly associated with the cell cycle, apoptosis, protein synthesis, and proteolysis.Conclusions: Puerarin has the potential to treat sarcopenia through the regulation of the cell cycle, apoptosis, and protein homeostasis. Our study has laid a foundation for further studies on drug development and pharmacological experiments in the treatment of sarcopenia.

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RETRACTED: The regulation of survival and differentiation of neural stem cells by miR-124 via modulating PAX3

Cited by 12 publications

References 23 publications

Regulation of GFAP Expression

Regulation of GFAP Expression

CHD7 promotes neural progenitor differentiation in embryonic stem cells via altered chromatin accessibility and nascent gene expression

Network pharmacology-based analysis of the effects of puerarin on sarcopenia

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