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Cited by 128

Control of oligodendroglial cell number by the miR-17-92 cluster

Budde, Holger, Schmitt, Sebastian, Fitzner, Dirk, Opitz, Lennart, Salinas-Riester, Gabriela, Simons, Mikael·2010·Development
DOI 10.1242/dev.050633
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Abstract

The generation of myelinating cells in the central nervous system requires the initiation of specific gene expression programs in oligodendrocytes. We reasoned that microRNAs (miRNAs) could play an important role in this process by regulating crucial developmental genes. Microarray profiling of cultured oligodendrocytes identified the miR-17-92 miRNA cluster as highly enriched in oligodendrocytes. We specifically deleted the miR-17-92 cluster in oligodendrocytes using 2′,3′-cyclic nucleotide 3′ phosphodiesterase (Cnp)-Cre mice. Absence of miR-17-92 leads to a reduction in oligodendrocyte number in vivo and we find that the expression of these miRNAs in primary cultures of oligodendrocyte precursor cells promotes cell proliferation by influencing Akt signaling. Together, these results suggest that the miRNA pathway is essential in determining oligodendroglial cell number and that the miR-17-92 cluster is crucial in this process.

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  • Some miR-17-92 members (miR-17-5p, 18a-5p, 19a-3p, 20a-5p, 19b-3p, and 92a-3p) have been implicated in the regulation of OPC proliferation in rodents, but their expression during postnatal brain development and cultured OPC differentiation has not been addressed.

    “Some of them (miR-17-5p, 18a-5p, 19a-3p, 20a-5p, 19b-3p, and 92a-3p, highlighted in red in Figure 4A) have been implicated in the regulation of OPC proliferation in rodents, but their expression during postnatal brain development and cultured OPC differentiation has not been addressed (Budde et al., 2010).”

    From Regulation of miRNA 219 and miRNA Clusters 338 and 17-92 in Oligodendrocytes (2012) · cites this paper as Budde et al., 2010

  • Expression profiling studies with rodent OLs have reported that several miR species are dramatically regulated during OPC differentiation.

    “Expression profiling studies with rodent OLs have reported that several miR species are dramatically regulated during OPC differentiation (Lau et al., 2008; Budde et al., 2010; Dugas et al., 2010).”

    From Regulation of miRNA 219 and miRNA Clusters 338 and 17-92 in Oligodendrocytes (2012) · cites this paper as Budde et al., 2010

  • Over-expression of miR-219-5p, miR-338-5p, and miR-338-3p promotes rodent OPC differentiation.

    “In these studies, over-expression of miR-219-5p, miR-338-5p, and miR-338-3p was shown to promote rodent OPC differentiation, indicating that these miRs play important roles during myelination (Lau et al., 2008; Budde et al., 2010; Dugas et al., 2010).”

    From Regulation of miRNA 219 and miRNA Clusters 338 and 17-92 in Oligodendrocytes (2012) · cites this paper as Budde et al., 2010

  • This data is consistent with the proposed role of the miR-17-92 cluster in the control of cell number.

    “This data is consistent with the proposed role of the miR-17-92 cluster in the control of cell number (Budde et al., 2010).”

    From Regulation of miRNA 219 and miRNA Clusters 338 and 17-92 in Oligodendrocytes (2012) · cites this paper as Budde et al., 2010

  • The dramatic downregulation is in agreement with their role in controlling OPC number.

    “We used quantitative real-time RT-PCR to study the expression of these miRs during mouse brain development and found a dramatic downregulation within the first postnatal week, in agreement with their role in controlling OPC number (Budde et al., 2010).”

    From Regulation of miRNA 219 and miRNA Clusters 338 and 17-92 in Oligodendrocytes (2012) · cites this paper as Budde et al., 2010

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Authors
Budde, H., Schmitt, S., Fitzner, D., Opitz, L., Salinas-Riester, G., & Simons, M.
Affiliations
  • Max Planck Institute for Experimental Medicine, Hermann-Rein-Strasse 3, D-37075 Göttingen, Germany.
  • Department of Biochemistry, University of Göttingen, D-37073 Göttingen, Germany.
Venue
Development
Publisher
The Company of Biologists
Published
2010-07-01
Volume
137
Issue
13
Pages
2127-2132
ISSN
  • 1477-9129
  • 0950-1991
DOI
10.1242/dev.050633
Cited by
128
References
4
Language
en

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