Method of increasing trafficking of endothelial progenitor cells to ischemia-damaged tissue

Abstract

This invention provides a method of increasing trafficking of endothelial progenitor cells to ischemia-damaged tissue in a subject comprising administering to the subject an agent that inhibits interaction between Stromal-Derived Factor-1 and CXCR-4.

Description

[0001] This application is a continuation-in-part and claims priority of U.S. Ser. No. 09 / 587,441, filed Jun. 5, 2000, the contents of which are hereby incorporated by reference.[0002] Throughout this application, various references are referred to within parentheses. Disclosures of these publications in their entireties are hereby incorporated by reference into this application to more fully describe the state of the art to which this invention pertains. Full bibliographic citation for these references may be found at the end of this application, preceding the claims. BACKGROUND OF THE INVENTION [0003] Left ventricular remodeling after myocardial infarction is a major cause of subsequent heart failure and death. The capillary network cannot keep pace with the greater demands of the hypertrophied but viable myocardium, resulting in myocardial death and fibrous replacement. The first series of experiments of the present invention, described below, show that human adult bone marrow co...

AI Technical Summary

Benefits of technology

[0061] This invention also provides a method for treating a cancer in a subject comprising administering to the subject a monoclonal antibody directed against an epitope of a specific chemokine produced by proliferating cells associated with the cancer so as to reduce trafficking of endothelial progenitor cells to such proliferating cells and thereby treat the cancer in the subject.

[0062] This invention also provides a method for treating a cancer in a subject comprising administering to the subject a monoclonal antibody directed against an epitope of a specific receptor located on an endothelial progenitor cell, for a chemokine produced by proliferating cells associated with the cancer, so as to reduce trafficking of the endothelial progenitor cell to such proliferating cells and thereby treat the cancer in the subject.

[0063] This invention also provides a method for treating a tumor in a subject comprising administering to the subject an antagonist to a specific receptor on an endothelial progenitor cell so as to reduce the progenitor cell's ability to induce vasculogenesis in the subject's tumor and thereby treat the tumor.

[0064] This invention also provides a method for treating a tumor in a subject comprising administering to the subject an antagonist to a specific receptor on an endothelial progenitor cell so as to reduce the progenitor cell's ability to induce angiogenesis in the subject's tumor and thereby treat the tumor.

[0090] (c) introducing the recovered cells into a different location in the subject such that the cells improve myocardial function in the subject.

Problems solved by technology

Left ventricular remodeling after myocardial infarction is a major cause of subsequent heart failure and death.

The capillary network cannot keep pace with the greater demands of the hypertrophied but viable myocardium, resulting in myocardial death and fibrous replacement.

However, the signals from ischemic sites required for chemoattraction of such bone marrow-derived precursors, and the receptors used by these cells for selective trafficking to these sites, are unknown.

This process, termed remodeling, results in progressive heart failure (67-69).

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