Transcriptomics

Dataset Information

471

MiR-221 is required for endothelial tip cell behaviors during vascular development


ABSTRACT: Through deep sequencing and functional screening in zebrafish, we find that miR-221 is essential for angiogenesis. miR-221 knockdown phenocopied defects associated with loss of the tip cell-expressed Flt4 receptor. Furthermore, miR-221 was required for tip cell proliferation and migration, as well as tip cell potential in mosaic blood vessels. miR-221 knockdown also prevented “hyper-angiogenesis” defects associated with Notch deficiency and miR-221 expression was inhibited by Notch signaling. Finally, miR-221 promoted tip cell behavior through repression of two targets: cyclin-dependent kinase inhibitor 1b (cdkn1b) and phosphoinositide-3-kinase regulatory subunit 1 (pik3r1). These results identify miR-221 as an important regulatory node through which tip cell migration and proliferation are controlled during angiogenesis. Identification of endothelial-expressed microRNA from FACS-isolated zebrafish endothelial cells.

ORGANISM(S): Danio rerio  

SUBMITTER: Stefania Nicoli   Nathan Lawson  Abirami Lakshmanan  Abirami Lakshmanan 

PROVIDER: E-GEOD-35078 | ArrayExpress | 2012-02-28

SECONDARY ACCESSION(S): GSE35078SRP010291PRJNA150927

REPOSITORIES: GEO, ArrayExpress, ENA

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miR-221 is required for endothelial tip cell behaviors during vascular development.

Nicoli Stefania S   Knyphausen Carl-Philipp CP   Zhu Lihua J LJ   Lakshmanan Abirami A   Lawson Nathan D ND  

Developmental cell 20120201 2


Angiogenesis requires coordination of distinct cell behaviors between tip and stalk cells. Although this process is governed by regulatory interactions between the vascular endothelial growth factor (Vegf) and Notch signaling pathways, little is known about the potential role of microRNAs. Through deep sequencing and functional screening in zebrafish, we find that miR-221 is essential for angiogenesis. miR-221 knockdown phenocopied defects associated with loss of the tip cell-expressed Flt4 rece  ...[more]

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