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Journal of Cellular Biochemistry

Role of ERK1/2 in platelet lysate-driven endothelial cell repair

Authors

  • Elia Ranzato,

    Corresponding author
    1. Department of Environment and Life Sciences, University of Piemonte Orientale “Amedeo Avogadro”, viale T. Michel 11, 15121 Alessandria, Italy
    2. Molecular Histology and Cell Growth Unit, San Raffaele Scientific Institute, via Olgettina 58, 20123 Milano, Italy
    • DiSAV, University of Piemonte Orientale “Amedeo Avogadro”, viale T. Michel 11, 15121 Alessandria, Italy.
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  • Francesca Boccafoschi,

    1. Clinical and Experimental Medicine Department, University of Piemonte Orientale “Amedeo Avogadro”, via Solaroli 17, 28100 Novara, Italy
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  • Laura Mazzucco,

    1. Department of Haematology & Blood Transfusion Medicine, Azienda Ospedaliera Nazionale SS. Antonio e Biagio e C. Arrigo, via Venezia 16, 15121 Alessandria, Italy
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  • Mauro Patrone,

    1. Department of Environment and Life Sciences, University of Piemonte Orientale “Amedeo Avogadro”, viale T. Michel 11, 15121 Alessandria, Italy
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  • Bruno Burlando

    1. Department of Environment and Life Sciences, University of Piemonte Orientale “Amedeo Avogadro”, viale T. Michel 11, 15121 Alessandria, Italy
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Abstract

Mechanisms of endothelial repair induced by a platelet lysate (PL) were studied on human (HuVEC, HMVEC-c) and non-human (PAOEC, bEnd5) endothelial cells. A first set of analyses on these cells showed that 20% (v/v) PL promotes scratch wound healing, with a maximum effect on HuVEC. Further analyses made on HuVEC showed that the ERK inhibitor PD98059 maximally inhibited the PL-induced endothelial repair, followed in order of importance by the calcium chelator BAPTA-AM, the PI3K inhibitor wortmannin and the p38 inhibitor SB203580. The PL exerted a chemotactic effect on HuVEC, which was abolished by all the above inhibitors, and induced a PD98059-sensitive increase of cell proliferation rate. Confocal calcium imaging of fluo-3-loaded HuVEC showed that PL was able to induce cytosolic free Ca2+ oscillations, visible also in Ca2+-free medium, suggesting an involvement of Ins3P-dependent Ca2+ release. Western blot analysis on scratch wounded HuVEC showed that PL induced no activation of p38, a transient activation of AKT, and a sustained activation of ERK1/2. The complex of data indicates that, although different signalling pathways are involved in PL-promoted endothelial repair, the process is chiefly under the control of ERK1/2. J. Cell. Biochem. 110: 783–793, 2010. © 2010 Wiley-Liss, Inc.

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