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J Thromb Haemost. 2012 Jun;10(6):1152-64. doi: 10.1111/j.1538-7836.2012.04710.x.

The recombinant bifunctional protein αCD133-GPVI promotes repair of the infarcted myocardium in mice.

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1
NMI, Natural and Medical Sciences Institute at the University of Tübingen, Regenerative Medicine I, Reutlingen University Clinic of Tübingen, Germany.

Abstract

BACKGROUND:

Bone-marrow-derived progenitor cells are important in myocardial repair mechanisms following prolonged ischemia. Cell-based therapy of diseased myocardium is limited by a low level of tissue engraftment.

OBJECTIVES:

The aim of this study was the development of the bifunctional protein αCD133-glycoprotein (GP)VI as an effective treatment for supporting vascular and myocardial repair mechanisms.

RESULTS:

We have generated and characterized a bifunctional molecule (αCD133-GPVI) that binds both to the subendothelium of the injured microvasculature and to CD133(+) progenitor cells with high affinity. αCD133-GPVI enhances progenitor cell adhesion to extracellular matrix proteins and differentiation into mature endothelial cells. In vivo studies showed that αCD133-GPVI favors adhesion of circulating progenitor cells to the injured vessel wall (intravital microscopy). Also, treatment of mice undergoing experimental myocardial infarction with αCD133-GPVI-labeled progenitor cells reduces infarction size and preserves myocardial function.

CONCLUSIONS:

The bifunctional trapping protein αCD133-GPVI represents a novel and promising therapeutic option for limiting heart failure of the ischemic myocardium.

[Indexed for MEDLINE]
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