The invention shows the use of miR-24 modulation to interfere with angiogenic signalling in vitro and in vivo. MiR-24 is triggering endothelial cell (EC) apoptosis via a signal cascade involving the mediators GATA2, PAK4 and others. This is also accompanied by a deficient angiogenic response. MiR-24 antagonism can block these detrimental effects. In a murine model of myocardial infarction (MI) reflecting ischemic disease, miR-24 expression is enhanced specially in cardiac ECs. Following MI, therapeutic intervention with a miR-24 specific antagonist lowered endogenous miR-24, preserved cardiac function and improved capillary density. The same pro-angiogenic effects were seen when implanting matrigel plugs to mice after treatment with miR-24 inhibitors. Thus, therapeutic knockdown of miR-24 is beneficial for cardiac performance upon MI and likely many other ischemic diseases. Collectively, miR-24 modulation can be useful in different settings of ischemic disease to sustain vasculature. As we have investigated therapeutic miR-24 intervention upon MI and in implanted matrigel plugs, we conclude that our results can be transferred to other ischemic stress models like hindlimb ischemia (peripheral occlusive disease), ischemic gut diseases, ischemia of virtually all organs such as kidney, liver, brain, spleen, dermal tissue, lung and others. In addition surgical operations and organ transplantation often result in ischemia-triggered organ function, which could be a target of miR-24 inhibitory therapies.
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