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AssigneeUniversity of Virginia Patent Foundation
InventorsBrian H. Annex, Charles R. Farber, Surovi Hazarika
Estimating the term…
The present application discloses roles for miR-93 in treating hypoxia and ischemia. Endothelial cells (HUVEC) and myocytes (C2C12) expressed miR-93 and up-regulated miR-93 in response to hypoxia and serum starvation. Over-expression of miR-93 in HUVECs promoted cell proliferation, prevented hypoxia-induced apoptosis, and enhanced endothelial cell tube formation. miR-93 knockdown in HUVECs resulted in increased hypoxia-induced apoptosis and decreased tube formation. Over-expression or knockdown of miR-93 in myocytes resulted in reduced or increased hypoxia-induced apoptosis, respectively. Down-regulation of miR-93 in C57BL/6 mice with antagomiR resulted in attenuated perfusion recovery (% non-ischemic leg at day-21: Scramble 85.22.9 vs. AntagomiR-93 67.96). Over-expression of miR-93 in BALB/C mice improved perfusion recovery (% non-ischemic leg at day 21: PremiR-93 757.5 vs. Scramble 59.62.5). The present invention encompasses the use of miR-93 and regulation of miR-93 to treat and prevent hypoxia, ischemia, and other injuries, diseases, disorders, and conditions associated with ischemia.
A method of treating or preventing a disease, disorder, injury, or condition associated with skeletal muscle ischemia, wherein said disease, disorder, injury, or condition is peripheral arterial disease, said method comprising administering to a subject a pharmaceutical composition comprising an effective amount of an agonist of miRNA expression, levels, or activity, a pharmaceutically-acceptable carrier, wherein said miRNA is miR-93, and optionally an additional therapeutic agent, thereby treating said disease, disorder, or condition associated with ischemia.
Dependencies are inferred from the claim text.