miR-137 forms a regulatory loop with nuclear receptor TLX and LSD1 in neural stem cells

Sun, Guoqiang; Ye, Peng; Murai, Kiyohito; Lang, Ming-Fei; Sheng-xiu, LI; Zhang, Heying; Li, Wendong; Fu, Chelsea; Yin, Jason Z.; Wang, Allen; Ma, Xiaoxiao; Shi, Yanhong

doi:10.1038/ncomms1532

Cited by 270 publications

(247 citation statements)

References 33 publications

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“…A number of studies have demonstrated the feasibility of this approach. For example, miR-137 mimics negatively regulate neural stem cell proliferation [120]. Additionally, miR-132 mimics have been shown to block ocular dominance plasticity produced by monocular deprivation when delivered to the mouse visual cortex [121].…”

Section: Microrna Therapymentioning

confidence: 99%

Epigenetics and ncRNAs in Brain Function and Disease: Mechanisms and Prospects for Therapy

2013

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The most fundamental roles of non-coding RNAs (ncRNAs) and epigenetic mechanisms are the guidance of cellular differentiation in development and the regulation of gene expression in adult tissues. In brain, both ncRNAs and the various epigenetic gene regulatory mechanisms play a fundamental role in neurogenesis and normal neuronal function. Thus, epigenetic chromatin remodelling can render coding sites transcriptionally inactive by DNA methylation, histone modifications or antisense RNA interactions. On the other hand, microRNAs (miRNAs) are ncRNA molecules that can regulate the expression of hundreds of genes post-transcriptionally, typically recognising binding sites in the 3′ untranslated region (UTR) of mRNA transcripts. Furthermore, there are a myriad of interactions in the interface of miRNAs and epigenetics. For example, epigenetic mechanisms can silence miRNA coding sites, and miRNAs can be the effectors of transcriptional gene silencing, targeting complementary promoters or silencing the expression of epigenetic modifier genes like MECP2 and EZH2 leading to global changes in the epigenome. Alterations in this regulatory machinery play a key role in the pathology of complex disorders including cancer and neurological diseases. For example, miRNA genes are frequently inactivated by epimutations in gliomas. Here we describe the interactions between epigenetic and ncRNA regulatory systems and discuss therapeutic potential, with an emphasis on tumors, cognitive disorders and neurodegenerative diseases.

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Section: Microrna Therapymentioning

confidence: 99%

Epigenetics and ncRNAs in Brain Function and Disease: Mechanisms and Prospects for Therapy

2013

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“…The overexpression of TRIM32 induces neuronal differentiation, whereas the inhibition of TRIM32 preserves the self-renewal capability of neural progenitor cells. The miRNA miR-137 is essential for embryonic NSC fate decisions; the overexpression of miR-137 inhibits NSC proliferation and induces accelerated differentiation by suppressing histone lysinespecific demethylase 1 (LSD1), a co-transcription factor of TLX [108] . Additionally, miR-137, which mediates epigenetic proteins such as MeCP2 (a DNA methylCpG-binding protein), Ezh2, and Polycomb group (PcG) protein, regulates the balance of NSC proliferation and differentiation in adult neurogenesis.…”

Section: Neuronal Differentiationmentioning

confidence: 99%

MicroRNAs as novel regulators of stem cell fate

Choi

Hwang³

2013

WJSC

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Mounting evidence in stem cell biology has shown that microRNAs (miRNAs) play a crucial role in cell fate specification, including stem cell self-renewal, lineagespecific differentiation, and somatic cell reprogramming. These functions are tightly regulated by specific gene expression patterns that involve miRNAs and transcription factors. To maintain stem cell pluripotency, specific miRNAs suppress transcription factors that promote differentiation, whereas to initiate differentiation, lineagespecific miRNAs are upregulated via the inhibition of transcription factors that promote self-renewal. Small molecules can be used in a similar manner as natural miRNAs, and a number of natural and synthetic small molecules have been isolated and developed to regulate stem cell fate. Using miRNAs as novel regulators of stem cell fate will provide insight into stem cell biology and aid in understanding the molecular mechanisms and crosstalk between miRNAs and stem cells.Ultimately, advances in the regulation of stem cell fate will contribute to the development of effective medical therapies for tissue repair and regeneration. This review summarizes the current insights into stem cell fate determination by miRNAs with a focus on stem cell self-renewal, differentiation, and reprogramming. Small molecules that control stem cell fate are also highlighted.© 2013 Baishideng. All rights reserved. Key words:MicroRNA; Stem cell fate; Differentiation; Self-renewal; Reprogramming; Small molecule Core tip: Stem cells are important in regenerative medicine applications due to their capacity to self-renew and differentiate into specific cell types. MicroRNAs (miRNAs) are short non-coding RNAs that negatively regulate gene expression at the post-transcriptional level. Recent studies suggest that miRNAs are key molecules in the regulation of stem cell fate decisions; this regulation is manifested as the fine tuning of cell-and tissue-specific gene expression. This review summarizes the current insights into stem cell fate determination by miRNAs and focuses on stem cell self-renewal, differentiation, and reprogramming. Small molecules that control stem cell fate are also highlighted.

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“…abundant in the brain, has an important role in controlling embryonic neural stem cell fate determination (32). The downregulated expression of miR-137 in brain cancer stem cells is necessary for self-renewal in glioma stem cells (33,34).…”

mentioning

confidence: 99%

MicroRNA-137 Is a Novel Hypoxia-responsive MicroRNA That Inhibits Mitophagy via Regulation of Two Mitophagy Receptors FUNDC1 and NIX

Wen

Zhang

Zhuang

et al. 2014

Journal of Biological Chemistry

118

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Background: Mitophagy and microRNA both regulate the occurrence of neurodegenerative diseases and cancers. Results: MicroRNA-137, a hypoxia responsive microRNA, inhibits mitophagy via targeting two mitophagy receptors. Conclusion: A novel link between miR-137 and mitophagy has been revealed. Significance: Understanding mitophagy regulation and microRNA functions may provide new concepts to fight human diseases.

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miR-137 forms a regulatory loop with nuclear receptor TLX and LSD1 in neural stem cells

Cited by 270 publications

References 33 publications

Epigenetics and ncRNAs in Brain Function and Disease: Mechanisms and Prospects for Therapy

Epigenetics and ncRNAs in Brain Function and Disease: Mechanisms and Prospects for Therapy

MicroRNAs as novel regulators of stem cell fate

MicroRNA-137 Is a Novel Hypoxia-responsive MicroRNA That Inhibits Mitophagy via Regulation of Two Mitophagy Receptors FUNDC1 and NIX

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