Stephan Gnerlich

University of Tübingen

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Meinrad Gawaz

University of Tübingen

Konstantinos Stellos

Heidelberg University

Boris Bigalke

Charité - Universitätsmedizin Berlin

Harald F. Langer

German Centre for Cardiovascular Research

Victoria Panagiota

Medizinische Hochschule Hannover

Tanja Schönberger

Boehringer Ingelheim (Germany)

Manuela Fahrleitner

University of Tübingen

Bjoern F. Kraemer

LMU Klinikum

Anke S. Lonsdorf

Heidelberg University

Sarah Gehring

University of Tübingen

Cooperative Institutions

University of Tübingen

Heidelberg University

University of Belgrade

Czech Academy of Sciences, Institute of Physiology

National Institutes of Health

Universidad Nacional Autónoma de México

University Hospital Heidelberg

Sichuan University

Tel Aviv University

Université Libre de Bruxelles

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Engagement of αIIbβ3 (GPIIb/IIIa) with ανβ3 Integrin Mediates Interaction of Melanoma Cells with Platelets

Journal of Biological Chemistry (2011)

Anke S. Lonsdorf Björn Krämer Manuela Fahrleitner Tanja Schönberger Stephan Gnerlich

Extravasation

Intravital microscopy

10.1074/jbc.m111.269811

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Citations (103)

Erratum

Cellular Physiology and Biochemistry (2012)

Karen K. S. Sunahara Paulina Sannomiya Joilson O. Martins Deyuan Li Mao-yun Xue

10.1159/000337613

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Binding of Oxidized Low-Density Lipoprotein on Circulating Platelets Is increased in Patients With Acute Coronary Syndromes and Induces Platelet Adhesion to Vascular Wall In Vivo—Brief Report

Arteriosclerosis Thrombosis and Vascular Biology (2012)

Konstantinos Stellos Manuela Sauter Manuela Fahrleitner Juliane Grimm Dimitrios Stakos

Hyperlipidemia is associated with platelet hyperactivity. In the present study, we evaluated the binding of oxidized low-density lipoprotein (oxLDL) on the surface of circulating platelets in patients with stable coronary artery disease and acute coronary syndromes and its possible association with platelet activation. Furthermore, the role of oxLDL binding on platelet adhesion to collagen and endothelial cells in vitro as well as after carotid ligation in mice was investigated.Using flow cytometry, patients with acute coronary syndromes (n=174) showed significantly enhanced oxLDL binding compared with patients with stable coronary artery disease (n=182; P=0.007). Platelet-bound oxLDL positively correlated with the degree of platelet activation (expression of P-selectin and activated fibrinogen receptor; P<0.001 for both). Plasma oxLDL was increased in patients with acute coronary syndromes compared with stable angina pectoris patients. Preincubation of isolated platelets with oxLDL, but not with native LDL, resulted in enhanced platelet adhesion to collagen and activated endothelial cells under high shear stress in vitro, as well as after carotid ligation in C57BL/6J mice and apolipoprotein E(-/-) mice fed a high cholesterol diet.Increased platelet-bound oxLDL in patients with acute coronary syndromes may play an important role in atherothrombosis, thus providing a potential future therapeutic target.

Platelet adhesion

Low-density lipoprotein

10.1161/atvbaha.111.244707

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Junctional Adhesion Molecule A Expressed on Human CD34 ⁺ Cells Promotes Adhesion on Vascular Wall and Differentiation Into Endothelial Progenitor Cells

Arteriosclerosis Thrombosis and Vascular Biology (2010)

Konstantinos Stellos Harald F. Langer Stephan Gnerlich Victoria Panagiota Angela Paul

To investigate the role of junctional adhesion molecule A (JAM-A) on adhesion and differentiation of human CD34(+) cells into endothelial progenitor cells.Tissue healing and vascular regeneration is a multistep process requiring firm adhesion of circulating progenitor cells to the vascular wall and their further differentiation into endothelial cells. The role of JAM-A in platelet-mediated adhesion of progenitor cells was investigated by adhesion assays in vitro and with the help of intravital fluorescence microscopy in mice. Preincubation of human CD34(+) progenitor cells with soluble JAM-A-Fc (sJAM-A-Fc) resulted in significantly decreased adhesion over immobilized platelets or inflammatory endothelium under high shear stress in vitro and after carotid ligation in vivo or ischemia/reperfusion injury in the microcirculation of mice. Human CD34(+) cells express JAM-A, as defined by flow cytometry and Western blot analysis. JAM-A mediates differentiation of CD34(+) cells to endothelial progenitor cells and facilitates CD34(+) cell-induced reendothelialization in vitro. Pretreatment of human CD34(+) cells with sJAM-A-Fc resulted in increased neointima formation 3 weeks after endothelial denudation in the carotid arteries of nonobese diabetic/severe combined immunodeficient mice.These results indicate that the expression of JAM-A on CD34(+) cells mediates adhesion to the vascular wall after injury and differentiation into endothelial progenitor cells, a mechanism potentially involved in vascular regeneration. Human CD34(+) cells express JAM-A, mediating their interaction with platelets and endothelial cells. Specifically, JAM-A expressed on human CD34(+) progenitor cells regulates their adhesion over immobilized platelets or inflammatory endothelium under high shear stress in vitro and after carotid ligation in vivo or ischemia/reperfusion injury in the microcirculation of mice. Moreover, it mediates differentiation of CD34(+) cells to endothelial progenitor cells and facilitates reendothelialization.

Vasculogenesis

10.1161/atvbaha.110.204370

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Citations (48)

Die Expression von Junctional Adhesion Molecule-A auf humanen CD34+ Zellen fördert deren Adhäsion und Differenzierung zu endothelialen Progenitorzellen

Stephan Gnerlich

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Expression of Junctional Adhesion Molecule-C on the Surface of Platelets Supports Adhesion, but not Differentiation, of Human CD34<sup>+</sup> Cells <i>in Vitro</i>

Cellular Physiology and Biochemistry (2012)

Konstantinos Stellos Victoria Panagiota Stephan Gnerlich Oliver Borst Boris Bigalke

Background: CD34+ progenitor cells play an important role in haematopoiesis and vascular homeostasis. The aim of the present study was to investigate the role of platelet-derived junctional adhesion molecule-C (JAM-C) in adhesion and differentiation of human CD34+ cells in vitro, as well as its association with platelet-derived P-selectin in patients with coronary artery disease. Methods and Results: Using flow cytometry we observed that JAM-C expression on the surface of washed platelets is increased after activation with thrombin receptor activating peptide-6 in vitro and correlated with platelet-derived P-selectin expression in patients with coronary artery disease (r=0.326, P=0.007). The role of JAM-C and its counter receptor Mac-1 in adhesion of human CD34+ cells over immobilized platelets was investigated by using a neutralizing soluble protein (sJAM-C-Fc) and a monoclonal antibody against JAM-C or integrin Mac-1 (CD11b/CD18). Treatment with soluble JAM-C-Fc or anti-JAM-C or anti-Mac-1, but not with control-Fc or IgG1, resulted in a significantly decreased adhesion of human CD34+ cells to platelets under static conditions (P<0.05). In order to validate our findings under high shear stress we performed flow chamber experiments. In a similar manner, inhibiting JAM-C interaction with Mac-1 resulted in a significantly decreased adhesion of CD34+ cells over immobilized platelets under high shear stress (P<0.05). Colony forming unit assays and coculture assays revealed that inhibition of JAM-C/Mac-1 axis did not influence the platelet-mediated differentiation of CD34+ cells to endothelial cells or to macrophages/foam cells. Conclusions: Taken together a platelet-derived JAM-C supports CD34+ cell adhesion, a mechanism potentially involved in homing as well as domiciliation of human CD34+ cells.

P-selectin

10.1159/000337596

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Engagement of alpha IIb beta 3 (GPIIb/IIIa) with alpha nu beta 3 Integrin Mediates Interaction of Melanoma Cells with Platelets A CONNECTION TO HEMATOGENOUS METASTASIS

Journal of Biological Chemistry (2012)

Anke S. Lonsdorf Bjoern F. Kraemer Manuela Fahrleitner Tanja Schoenberger Stephan Gnerlich

Alpha (finance)

BETA (programming language)

Alpha-v beta-3

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