MicroRNA-130b targets Fmr1 and regulates embryonic neural progenitor cell proliferation and differentiation

https://doi.org/10.1016/j.bbrc.2013.08.096Get rights and content
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Highlights

  • We found that the 3′ UTR of the Fmr1 mRNA is a target of miR-130b.

  • MiR-130b suppresses the expression of Fmr1 in mouse embryonic stem cell.

  • MiR-130b alters the proliferation of mouse embryonic stem cell.

  • MiR-130b alters fate specification of mouse embryonic stem cell.

Abstract

Fragile X syndrome, one of the most common forms of inherited mental retardation, is caused by expansion of the CGG repeat in the 5′-untranslated region of the X-linked Fmr1 gene, which results in transcriptional silencing and loss of expression of its encoded protein FMRP. The loss of FMRP increases proliferation and alters fate specification in adult neural progenitor cells (aNPCs). However, little is known about Fmr1 mRNA regulation at the transcriptional and post-transcriptional levels. In the present study, we report that miR-130b regulated Fmr1 expression by directly targeting its 3′-untranslated region (3′ UTR). Up-regulation of miR-130b in mouse embryonic neural progenitor cells (eNPCs) decreased Fmr1 expression, markedly increased eNPC proliferation and altered the differentiation tendency of eNPCs, suggesting that antagonizing miR-130b may be a new therapeutic entry point for treating Fragile X syndrome.

Keywords

Fmr1
miR-130b
Proliferation
Differentiation
Neural progenitor cells

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