Journal
SCIENCE
Volume 324, Issue 5935, Pages 1710-1713Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1174381
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Funding
- Deutsche Forschungsgemeinschaft [Di 600/6-3, Exc 147/1]
- Alfried Krupp Foundation
- Landes-Offensive zur Entwicklung Wissenschaftlich-okonomischer Exzellenz (LOEWE)
- European Research Council (Angiomir)
- Leducq Foundation
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MicroRNAs (miRs) are small noncoding RNAs that regulate gene expression by binding to target messenger RNAs (mRNAs), leading to translational repression or degradation. Here, we show that the miR-17 similar to 92 cluster is highly expressed in human endothelial cells and that miR-92a, a component of this cluster, controls the growth of new blood vessels (angiogenesis). Forced overexpression of miR-92a in endothelial cells blocked angiogenesis in vitro and in vivo. In mouse models of limb ischemia and myocardial infarction, systemic administration of an antagomir designed to inhibit miR-92a led to enhanced blood vessel growth and functional recovery of damaged tissue. MiR-92a appears to target mRNAs corresponding to several proangiogenic proteins, including the integrin subunit alpha5. Thus, miR-92a may serve as a valuable therapeutic target in the setting of ischemic disease.
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