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

Publikation: Beiträge in ZeitschriftenZeitschriftenaufsätzeForschungbegutachtet


  • Yvonne Baumer
  • Christoph Leder
  • Melanie Ziegler
  • Tanja Schönberger
  • Carmen Ochmann
  • A. Perk
  • Heidrun Degen
  • Barbara Schmid-Horch
  • Margitta Elvers
  • Götz Münch
  • Marius Ungerer
  • Burkhard Schlosshauer
  • Meinrad Gawaz

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.

ZeitschriftJournal of Thrombosis and Haemostasis
Seiten (von - bis)1152-1164
Anzahl der Seiten13
PublikationsstatusErschienen - 06.2012