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

Publikation: Beiträge in Zeitschriften › Zeitschriftenaufsätze › Forschung › begutachtet

Standard

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

Harvard

Baumer, Y, Leder, C, Ziegler , M, Schönberger, T, Ochmann, C, Perk, A, Degen, H, Schmid-Horch, B, Elvers, M, Münch, G, Ungerer, M, Schlosshauer, B & Gawaz, M 2012, 'The recombinant bifunctional protein αCD133–GPVI promotes repair of the infarcted myocardium in mice', Journal of Thrombosis and Haemostasis , Jg. 10, Nr. 6, S. 1152-1164. https://doi.org/10.1111/j.1538-7836.2012.04710.x

APA

Baumer, Y., Leder, C., Ziegler , M., Schönberger, T., Ochmann, C., Perk, A., Degen, H., Schmid-Horch, B., Elvers, M., Münch, G., Ungerer, M., Schlosshauer, B., & Gawaz, M. (2012). The recombinant bifunctional protein αCD133–GPVI promotes repair of the infarcted myocardium in mice. Journal of Thrombosis and Haemostasis , 10(6), 1152-1164. https://doi.org/10.1111/j.1538-7836.2012.04710.x

Vancouver

Baumer Y, Leder C, Ziegler M, Schönberger T, Ochmann C, Perk A et al. The recombinant bifunctional protein αCD133–GPVI promotes repair of the infarcted myocardium in mice. Journal of Thrombosis and Haemostasis . 2012 Jun;10(6):1152-1164. doi: 10.1111/j.1538-7836.2012.04710.x

Bibtex

@article{14779e0103b64e24a28f7d5315eea844,
title = "The recombinant bifunctional protein αCD133–GPVI promotes repair of the infarcted myocardium in mice",
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.",
keywords = "Health sciences, CD133, glycoprotein VI, myocardial infarction, platelets, progenitor cells, Sustainability Science",
author = "Yvonne Baumer and Christoph Leder and Melanie Ziegler and Tanja Sch{\"o}nberger and Carmen Ochmann and A. Perk and Heidrun Degen and Barbara Schmid-Horch and Margitta Elvers and G{\"o}tz M{\"u}nch and Marius Ungerer and Burkhard Schlosshauer and Meinrad Gawaz",
year = "2012",
month = jun,
doi = "10.1111/j.1538-7836.2012.04710.x",
language = "English",
volume = "10",
pages = "1152--1164",
journal = "Journal of Thrombosis and Haemostasis ",
issn = "1538-7836",
publisher = "Wiley-Blackwell Publishing, Inc.",
number = "6",

}

RIS

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 - 1538-7836

IS - 6

ER -

DOI