Regulation of vascular endothelium using BMX tyrosine kinase
OwnerNiklas Ekman, Elena Arighi +3inventors
InventorsNiklas Ekman, Elena Arighi, Imre Vastrik, Luca Tamagnone, Kari Alitalo
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Abstract
Vascular endothelia are subject to atherosclerotic and arteriostenotic effects transduced by molecules, such as thrombin, IL-3 and VEGF which can lead to vessel occlusion or stenosis. An endothelial signaling pathway involving the Bmx tyrosine kinase contributes to normal endothelial nonthrombogenic, inflammatory and growth conditions of arterial vessels, and regulation of the pathway can treat or prevent pathological conditions in the vessel walls.
Claims23
A method of treating or preventing arteriostenosis in a patient comprising regulating Bmx tyrosine, kinase activity in endocardial and arterial endothelial cells in a manner sufficient to regulate growth signals in endothelium or adjacent smooth muscle, to regulate inflammatory response, or to improve the non-thrombogenic properties of vascular endothelium.
A method of inhibiting a thrombotic, mitotic, or inflammatory effect in vascular endothelium comprising regulating Bmx tyrosine kinase activity in endocardial and arterial endothelial cells.
A method of identifying agents which affect a Bmx tyrosine kinase signaling pathway comprising applying a test agent to tissue from a transgenic animal or administering the test agent to the transgenic animal, the cells of the animal having a genetic defect in the Bmx encoding region, the defect causing an abnormal Bmx signaling pathway, wherein an agent affecting the Bmx signaling pathway is one which functionally restores at least one step in the abnormal pathway.
A method for diagnosing a human disease associated with Bmx dysfunction due to mutation in the BMX gene on chromosome X of a patient comprising assaying the BMX gene on the X chromosome of a patient and analyzing the result of the assay to detect the mutation.
A method of accelerating re-endothelialization of damaged arterial or endocardial walls comprising regulation of Bmx tyrosine kinase activity in endocardial and arterial endothelial cells in a manner sufficient to enhance growth signals in the endothelium.
Dependencies are inferred from the claim text.