Platelet derived bFGF mediates vascular integrative mechanisms of mesenchymal stem cells in vitro
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Platelet derived bFGF mediates vascular integrative mechanisms of mesenchymal stem cells in vitro. / Langer, Harald F; Stellos, Konstantinos; Steingen, Caroline; Froihofer, Amrei; Schönberger, Tanja; Krämer, Björn; Bigalke, Boris; May, Andreas E; Seizer, Peter; Müller, Iris; Gieseke, Friederike; Siegel-Axel, Dorothea; Meuth, Sven G; Schmidt, Annette; Wendel, Hans P; Müller, Ingo; Bloch, Wilhelm; Gawaz, Meinrad.
in: J MOL CELL CARDIOL, Jahrgang 47, Nr. 2, 08.2009, S. 315-25.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Platelet derived bFGF mediates vascular integrative mechanisms of mesenchymal stem cells in vitro
AU - Langer, Harald F
AU - Stellos, Konstantinos
AU - Steingen, Caroline
AU - Froihofer, Amrei
AU - Schönberger, Tanja
AU - Krämer, Björn
AU - Bigalke, Boris
AU - May, Andreas E
AU - Seizer, Peter
AU - Müller, Iris
AU - Gieseke, Friederike
AU - Siegel-Axel, Dorothea
AU - Meuth, Sven G
AU - Schmidt, Annette
AU - Wendel, Hans P
AU - Müller, Ingo
AU - Bloch, Wilhelm
AU - Gawaz, Meinrad
PY - 2009/8
Y1 - 2009/8
N2 - Patients with myocardial infarction reveal an altered number of circulating mesenchymal stem cells (MSCs). Recently, it was shown that MSCs are able to regenerate myocardial tissue and to differentiate into endothelial cells. The homing mechanisms of MSCs from the circulation into the target tissue, however, are not understood so far. In this study, we evaluated the impact of platelets on MSC recruitment, proliferation, migration and integration into the endothelium. MSCs expressing alpha(v)beta(3) integrin were recruited to human arterial endothelial cells exposed to isolated platelets or IL-1 beta under high shear conditions. Furthermore, induction of vascular injury in vivo resulted in increased recruitment of injected MSCs as assessed by intravital microscopy and depletion of platelets significantly reduced this adhesion. The interaction of platelets and MSCs was inhibited by pre-incubation with the mAb 7E3 or an RGD protein both blocking beta(3) integrin mediated adhesion. Platelets had a chemotactic effect on MSCs, promoted a migratory MSC phenotype and dose- and activation-dependently enhanced migration of MSCs, a process, which was mediated by basic fibroblast growth factor (bFGF). Similarly, platelet derived bFGF increased proliferation of MSCs. Coincubation of MSCs with platelets facilitated integration into an endothelial monolayer, which was significantly reduced by pre-incubation with a blocking mAb to bFGF. We conclude that platelets may play a critical part in the recruitment of MSCs to the endothelium, influence MSC function and promote integration of MSCs into the endothelium.
AB - Patients with myocardial infarction reveal an altered number of circulating mesenchymal stem cells (MSCs). Recently, it was shown that MSCs are able to regenerate myocardial tissue and to differentiate into endothelial cells. The homing mechanisms of MSCs from the circulation into the target tissue, however, are not understood so far. In this study, we evaluated the impact of platelets on MSC recruitment, proliferation, migration and integration into the endothelium. MSCs expressing alpha(v)beta(3) integrin were recruited to human arterial endothelial cells exposed to isolated platelets or IL-1 beta under high shear conditions. Furthermore, induction of vascular injury in vivo resulted in increased recruitment of injected MSCs as assessed by intravital microscopy and depletion of platelets significantly reduced this adhesion. The interaction of platelets and MSCs was inhibited by pre-incubation with the mAb 7E3 or an RGD protein both blocking beta(3) integrin mediated adhesion. Platelets had a chemotactic effect on MSCs, promoted a migratory MSC phenotype and dose- and activation-dependently enhanced migration of MSCs, a process, which was mediated by basic fibroblast growth factor (bFGF). Similarly, platelet derived bFGF increased proliferation of MSCs. Coincubation of MSCs with platelets facilitated integration into an endothelial monolayer, which was significantly reduced by pre-incubation with a blocking mAb to bFGF. We conclude that platelets may play a critical part in the recruitment of MSCs to the endothelium, influence MSC function and promote integration of MSCs into the endothelium.
KW - Animals
KW - Arteries
KW - Blood Platelets
KW - Blood Vessels
KW - Cell Adhesion
KW - Cell Movement
KW - Cell Proliferation
KW - Endothelial Cells
KW - Fibroblast Growth Factor 2
KW - Humans
KW - Integrin alphaVbeta3
KW - Mesenchymal Stromal Cells
KW - Mice
KW - Shear Strength
U2 - 10.1016/j.yjmcc.2009.03.011
DO - 10.1016/j.yjmcc.2009.03.011
M3 - SCORING: Journal article
C2 - 19328809
VL - 47
SP - 315
EP - 325
JO - J MOL CELL CARDIOL
JF - J MOL CELL CARDIOL
SN - 0022-2828
IS - 2
ER -