The recombinant bifunctional protein αCD133–GPVI promotes repair of the infarcted myocardium in mice
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The recombinant bifunctional protein αCD133–GPVI promotes repair of the infarcted myocardium in mice. / Baumer, Yvonne; Leder, Christoph; Ziegler , Melanie et al.
in: Journal of Thrombosis and Haemostasis , Jahrgang 10, Nr. 6, 06.2012, S. 1152-1164.Publikation: Beiträge in Zeitschriften › Zeitschriftenaufsätze › Forschung › begutachtet
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TY - JOUR
T1 - The recombinant bifunctional protein αCD133–GPVI promotes repair of the infarcted myocardium in mice
AU - Baumer, Yvonne
AU - Leder, Christoph
AU - Ziegler , Melanie
AU - Schönberger, Tanja
AU - Ochmann, Carmen
AU - Perk, A.
AU - Degen, Heidrun
AU - Schmid-Horch, Barbara
AU - Elvers, Margitta
AU - Münch, Götz
AU - Ungerer, Marius
AU - Schlosshauer, Burkhard
AU - Gawaz, Meinrad
PY - 2012/6
Y1 - 2012/6
N2 - 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.
AB - 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.
KW - Health sciences
KW - CD133
KW - glycoprotein VI
KW - myocardial infarction
KW - platelets
KW - progenitor cells
KW - Sustainability Science
UR - http://www.scopus.com/inward/record.url?scp=84861657646&partnerID=8YFLogxK
U2 - 10.1111/j.1538-7836.2012.04710.x
DO - 10.1111/j.1538-7836.2012.04710.x
M3 - Journal articles
C2 - 22448969
VL - 10
SP - 1152
EP - 1164
JO - Journal of Thrombosis and Haemostasis
JF - Journal of Thrombosis and Haemostasis
SN - 1538-7933
IS - 6
ER -