Role of microRNAs in central nervous system development and pathology

Meza-Sosa, Karla F.; Valle-García, David; Pedraza‐Alva, Gustavo; Pérez-Martı́nez, Leonor

doi:10.1002/jnr.22701

Cited by 91 publications

(90 citation statements)

References 92 publications

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“…From this list, we searched for any that were known to be expressed in cortical progenitors in a complementary pattern to Tbr2. Neural progenitor cells were known to express miR-92b and, although its physiological target was not known (20)(21)(22), one publication highlighted it as an interesting candidate because its expression decreases as Tbr2 expression increases during development (20). TargetScan (www.targetscan.org) and microRNA.org both predicted the presence of a single highly conserved site complementary to the seed region of miR-92b in the 3′UTR of the mouse Tbr2 mRNA between nucleotides 2707-2714 ( Fig.…”

Section: Mir-92b Overexpression Causes a Rapid Reduction Of Intermediatementioning

confidence: 99%

MicroRNA-92b regulates the development of intermediate cortical progenitors in embryonic mouse brain

Nowakowski

Fotaki

Pollock

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Cerebral cortical neurons arise from radial glia (direct neurogenesis) or from intermediate progenitors (indirect neurogenesis); intriguingly, the sizes of intermediate progenitor populations and the cortices they generate correlate across species. The generation of intermediate progenitors is regulated by the transcription factor Tbr2, whose expression marks these cells. We investigated how this mechanism might be controlled. We found that acute blockade of mature microRNA biosynthesis in murine cortical progenitors caused a rapid cell autonomous increase in numbers of Tbr2-expressing cells. Acute microRNA-92b (miR-92b) gain of function caused rapid reductions in numbers of Tbr2-expressing cells and proliferating intermediate progenitors. Acute miR-92b loss of function had opposite effects. These findings indicate that miR-92b limits the production of intermediate cortical progenitors.cortical development | microRNAs

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Section: Mir-92b Overexpression Causes a Rapid Reduction Of Intermediatementioning

confidence: 99%

MicroRNA-92b regulates the development of intermediate cortical progenitors in embryonic mouse brain

Nowakowski

Fotaki

Pollock

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…Some studies have shown roles for miRNAs in neuronal development and differentiation [30,31,32,33,34]. Maternal-zygotic Dicer mutant zebrafish that lack all mature miRNAs display abnormal brain morphogenesis and neural differentiation [35].…”

Section: Mirnas In the Cnsmentioning

confidence: 99%

MicroRNAs in the Hypothalamus

2013

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MicroRNAs (miRNAs) are short (∼22 nucleotides) non-coding ribonucleic acid (RNA) molecules that negatively regulate the expression of protein-coding genes. Posttranscriptional silencing of target genes by miRNA is initiated by binding to the 3′-untranslated regions of target mRNAs, resulting in specific cleavage and subsequent degradation of the mRNA or by translational repression resulting in specific inhibition of protein synthesis. An increasing amount of evidence shows that miRNAs control a large number of biological processes and there exists a direct link between miRNAs and disease. miRNA molecules are abundantly expressed in tissue-specific and regional patterns and have been suggested as potential biomarkers, disease modulators and drug targets. The central nervous system is a prominent site of miRNA expression. Within the brain, several miRNAs are expressed and/or enriched in the region of the hypothalamus and miRNAs have recently been shown to be important regulators of hypothalamic control functions. The aim of this review is to summarize some of the current knowledge regarding the expression and role of miRNAs in the hypothalamus.

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“…As one of chronic autoimmune diseases, human MS is also a multiple genetic disease characterized by inflammation and demyelination in CNS. In consideration of the importance of the proper regulation by miRNAs for specific gene expressing and normal function during CNS development (25), recently, many groups have identified miRNA expression-profiling patterns in PBMCs, lymphocytes, serum, and whole blood in different MS subtype patients compared with healthy controls (26). Interestingly, the abnormal expression and function of several miRNAs that identified deregulated in MS patients were also found in EAE model and required Th17 cell participation.…”

mentioning

confidence: 99%

miR-20b Suppresses Th17 Differentiation and the Pathogenesis of Experimental Autoimmune Encephalomyelitis by Targeting RORγt and STAT3

Zhu

Zheng

et al. 2014

The Journal of Immunology

113

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The differentiation and function of IL-17–producing Th17 cells are tightly regulated by specific transcription factors and cytokines, which are the key participants in the pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Although specific miRNAs have been shown to be involved in the development of MS and EAE, the potential role of miRNAs in the context of Th17-driven autoimmunity is just beginning to be clarified. miR-20b has been reported as a downregulated miRNA in blood cells of MS patients. In this report, it was further studied in greater detail because we found it was significantly downregulated during EAE, and, in the in vitro differentiation model, Th17 cells had lower expression of miR-20b than did Th1, Th2, or inducible T regulatory cells. Ectopic expression of miR-20b repressed Th17 differentiation in vitro. Using lentiviral vectors for miR-20b overexpression in vivo, we demonstrated that overexpression of miR-20b led to decreased Th17 cells and reduced severity of EAE. Furthermore, we also identified both RAR-related orphan receptor γt and STAT3 as potential targets of miR-20b. Finally, we confirmed that the mild disease severity and low number of Th17 cells in LV-miR-20b–infected mice were largely reversed by coinfection of these mice with lentivirus-expressing RAR-related orphan receptor γt or STAT3 3′-untranslated regions. Taken together, our results contribute to the importance of miRNAs in Th17 differentiation and pathogenesis of MS and EAE.

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Role of microRNAs in central nervous system development and pathology

Cited by 91 publications

References 92 publications

MicroRNA-92b regulates the development of intermediate cortical progenitors in embryonic mouse brain

MicroRNA-92b regulates the development of intermediate cortical progenitors in embryonic mouse brain

MicroRNAs in the Hypothalamus

miR-20b Suppresses Th17 Differentiation and the Pathogenesis of Experimental Autoimmune Encephalomyelitis by Targeting RORγt and STAT3

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