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Status |
Public on Feb 28, 2012 |
Title |
miR-221 is required for endothelial tip cell behaviors during vascular development |
Organism |
Danio rerio |
Experiment type |
Non-coding RNA profiling by high throughput sequencing
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Summary |
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.
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Overall design |
Identification of endothelial-expressed microRNA from FACS-isolated zebrafish endothelial cells.
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Contributor(s) |
Lakshmanan A, Lawson N, Nicoli S |
Citation(s) |
22340502 |
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Submission date |
Jan 12, 2012 |
Last update date |
May 15, 2019 |
Contact name |
Abirami Lakshmanan |
E-mail(s) |
abirami.lakshmanan@umassmed.edu
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Organization name |
Umass Medical School
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Department |
PGFE
|
Lab |
Nathan Lawson Lab
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Street address |
55 Lake Avenue North
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City |
Worcester |
State/province |
Massachusetts |
ZIP/Postal code |
01655 |
Country |
USA |
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Platforms (1) |
GPL10164 |
Illumina Genome Analyzer (Danio rerio) |
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Samples (3) |
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Relations |
SRA |
SRP010291 |
BioProject |
PRJNA150927 |