期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 105, 期 37, 页码 14082-14087出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0804597105
关键词
endothelium; VEGF
资金
- National Institute of Health [R01 HL64793, R01 HL61371, R01 HL57665, PO1 HL70295]
- National Heart, Lung, and Blood Institute [N01-HV-28186]
- Centro Nacional de Investigaciones Cardiovasculares
- American Heart Association
- Phillip Morris USA
- MRC [MC_U120027516] Funding Source: UKRI
- Medical Research Council [MC_U120027516] Funding Source: researchfish
Posttranscriptional gene regulation by microRNAs (miRNAs) is important for many aspects of development, homeostasis, and disease. Here, we show that reduction of endothelial miRNAs by cell-specific inactivation of Dicer, the terminal endonuclease responsible for the generation of miRNAs, reduces postnatal angiogenic response to a variety of stimuli, including exogenous VEGF, tumors, limb ischemia, and wound healing. Furthermore, VEGF regulated the expression of several miRNAs including the up-regulation of components of the c-Myc oncogenic cluster miR-17-92. Transfection of endothelial cells with components of the miR-17-92 cluster, induced by VEGF treatment, rescued the induced expression of thrombospondin-1 and the defect in endothelial cell proliferation and morphogenesis initiated by the loss of Dicer. Thus, endothelial miRNAs regulate postnatal angiogenesis and VEGF induces the expression of miRNAs implicated in the regulation of an integrated angiogenic response.
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