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Discovery of microvascular miRNAs using public gene expression data: miR-145 is expressed in pericytes and is a regulator of Fli1.

Artikel i vetenskaplig tidskrift
Författare Erik Larsson
Peder Fredlund Fuchs
Johan Heldin
Irmeli Barkefors
Cecilia Bondjers
Guillem Genové
Christelle Arrondel
Pär Gerwins
Christine Kurschat
Bernhard Schermer
Thomas Benzing
Scott J Harvey
Johan Kreuger
Per Lindahl
Publicerad i Genome medicine
Volym 1
Nummer/häfte 11
Sidor 108
ISSN 1756-994X
Publiceringsår 2009
Publicerad vid Wallenberglaboratoriet
Institutionen för biomedicin
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 108
Språk en
Länkar dx.doi.org/10.1186/gm108
Ämneskategorier Medicinsk cellbiologi

Sammanfattning

ABSTRACT: BACKGROUND: A function for the microRNA (miRNA) pathway in vascular development and angiogenesis has been firmly established. miRNAs with selective expression in the vasculature are attractive as possible targets in miRNA-based therapies. However, little is known about the expression of miRNAs in microvessels in vivo. Here, we identified candidate microvascular-selective miRNAs by screening public miRNA expression datasets. METHODS: Bioinformatics predictions of microvascular-selective expression were validated with real-time quantitative reverse transcription PCR on purified microvascular fragments from mouse. Pericyte expression was shown with in situ hybridization on tissue sections. Target sites were identified with 3' UTR luciferase assays, and migration was tested in a microfluid chemotaxis chamber. RESULTS: miR-145, miR-126, miR-24, and miR-23a were selectively expressed in microvascular fragments isolated from a range of tissues. In situ hybridization and analysis of Pdgfb retention motif mutant mice demonstrated predominant expression of miR-145 in pericytes. We identified the Ets transcription factor Friend leukemia virus integration 1 (Fli1) as a miR-145 target, and showed that elevated levels of miR-145 reduced migration of microvascular cells in response to growth factor gradients in vitro. CONCLUSIONS: miR-126, miR-24 and miR-23a are selectively expressed in microvascular endothelial cells in vivo, whereas miR-145 is expressed in pericytes. miR-145 targets the hematopoietic transcription factor Fli1 and blocks migration in response to growth factor gradients. Our findings have implications for vascular disease and provide necessary information for future drug design against miRNAs with selective expression in the microvasculature.

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