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Members of the microRNA-17-92 cluster exhibit a cell-intrinsic antiangiogenic function in endothelial cells

MicroRNAs are endogenously expressed small noncoding RNAs that regulate gene expression on the posttranscriptional level. The miR-17-92 cluster (encoding miR-17, -18a, -19a/b, -20a, and miR-92a) is highly expressed in tumor cells and is up-regulated by ischemia. Whereas miR-92a was recently identifi...

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Main Authors: Döbele, Carmen (Author) , Bonauer, Angelika (Author) , Fischer, Ariane (Author) , Scholz, Alexander (Author) , Reiss, Yvonne (Author) , Urbich, Carmen (Author) , Hofmann, Wolf-Karsten (Author) , Zeiher, Andreas M. (Author) , Dimmeler, Stefanie (Author)
Format: Article (Journal)
Language:English
Published: March 18, 2010
In: Blood
Year: 2010, Volume: 115, Issue: 23, Pages: 4944-4950
ISSN:1528-0020
DOI:10.1182/blood-2010-01-264812
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1182/blood-2010-01-264812
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Author Notes:Carmen Doebele, Angelika Bonauer, Ariane Fischer, Alexander Scholz, Yvonne Reiss, Carmen Urbich, Wolf-Karsten Hofmann, Andreas M. Zeiher, and Stefanie Dimmeler

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520 |a MicroRNAs are endogenously expressed small noncoding RNAs that regulate gene expression on the posttranscriptional level. The miR-17-92 cluster (encoding miR-17, -18a, -19a/b, -20a, and miR-92a) is highly expressed in tumor cells and is up-regulated by ischemia. Whereas miR-92a was recently identified as negative regulator of angiogenesis, the specific functions of the other members of the cluster are less clear. Here we demonstrate that overexpression of miR-17, -18a, -19a, and -20a significantly inhibited 3-dimensional spheroid sprouting in vitro, whereas inhibition of miR-17, -18a, and -20a augmented endothelial cell sprout formation. Inhibition of miR-17 and miR-20a in vivo using antagomirs significantly increased the number of perfused vessels in Matrigel plugs, whereas antagomirs that specifically target miR-18a and miR-19a were less effective. However, systemic inhibition of miR-17/20 did not affect tumor angiogenesis. Further mechanistic studies showed that miR-17/20 targets several proangiogenic genes. Specifically, Janus kinase 1 was shown to be a direct target of miR-17. In summary, we show that miR-17/20 exhibit a cell-intrinsic antiangiogenic activity in endothelial cells. Inhibition of miR-17/20 specifically augmented neovascularization of Matrigel plugs but did not affect tumor angiogenesis indicating a context-dependent regulation of angiogenesis by miR-17/20 in vivo. 
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