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Role of ERK1/2 in platelet lysate‐driven endothelial cell repair
Author(s) -
Ranzato Elia,
Boccafoschi Francesca,
Mazzucco Laura,
Patrone Mauro,
Burlando Bruno
Publication year - 2010
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22591
Subject(s) - wortmannin , microbiology and biotechnology , endothelial stem cell , bapta , chemistry , mapk/erk pathway , p38 mitogen activated protein kinases , cell migration , wound healing , pi3k/akt/mtor pathway , western blot , cell , biology , signal transduction , immunology , biochemistry , in vitro , intracellular , gene
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 Ca 2+ oscillations, visible also in Ca 2+ ‐free medium, suggesting an involvement of Ins3P‐dependent Ca 2+ 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.