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Therefore, they represent a suitable tool for cell-based therapy (CBT) in regenerative medicine and provide a novel promising target in the fight against cancer. Intracellular Ca2+ signals regulate numerous endothelial functions, such as proliferation and tubulogenesis. The growth of endothelial colony forming cells (ECFCs), which are EPCs capable of acquiring a mature endothelial phenotype, is governed by store-dependent Ca2+ entry (SOCE). This study aimed at investigating the nature and the role of VEGF-elicited Ca2+ signals in ECFCs. VEGF induced asynchronous Ca2+ oscillations, whose latency, amplitude, and frequency were correlated to the growth factor dose. Removal of external Ca2+ (0Ca2+) and SOCE inhibition with N-(4-[3,5-bis(trifluoromethyl)-1H-pyrazol-1-yl]phenyl)-4-methyl-1,2,3-thiadiazole-5-carboxamide (BTP-2) reduced the duration of the oscillatory signal. Blockade of phospholipase C-\u03b3 with U73122, emptying the inositol-1,4,5-trisphosphate (InsP3)-sensitive Ca2+ pools with cyclopiazonic acid (CPA), and inhibition of InsP3 receptors with 2-APB prevented the Ca2+ response to VEGF. VEGF-induced ECFC proliferation and tubulogenesis were inhibited by the Ca2+-chelant, BAPTA, and BTP-2. NF-\u03baB activation by VEGF was impaired by BAPTA, BTP-2, and its selective blocker, thymoquinone. Thymoquinone, in turn, suppressed VEGF-dependent ECFC proliferation and tubulogenesis. These data indicate that VEGF-induced Ca2+ oscillations require the interplay between InsP3-dependent Ca2+ release and SOCE, and promote ECFC growth and tubulogenesis by engaging NF-\u03baB. This novel signaling pathway might be exploited to enhance the outcome of CBT and chemotherapy.<\/jats:p>","DOI":"10.1002\/stem.734","type":"journal-article","created":{"date-parts":[[2011,9,8]],"date-time":"2011-09-08T11:26:07Z","timestamp":1315481167000},"page":"1898-1907","source":"Crossref","is-referenced-by-count":143,"title":["Vascular Endothelial Growth Factor Stimulates Endothelial Colony Forming Cells Proliferation and Tubulogenesis by Inducing Oscillations in Intracellular Ca2+ Concentration"],"prefix":"10.1093","volume":"29","author":[{"given":"Silvia","family":"Dragoni","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Pavia, Pavia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Umberto","family":"Laforenza","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Pavia, Pavia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisa","family":"Bonetti","sequence":"additional","affiliation":[{"name":"Unit of Clinical Epidemiology, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francesco","family":"Lodola","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Pavia, Pavia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cinzia","family":"Bottino","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Pavia, Pavia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roberto","family":"Berra-Romani","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, School of Medicine, Benem\u00e9rita Universidad Aut\u00f3noma de Puebla, Colonia Volcanes, Puebla, M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giacomo","family":"Carlo Bongio","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Pavia, Pavia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Pia","family":"Cinelli","sequence":"additional","affiliation":[{"name":"Department of Biomorphological and Functional Sciences, Via Pansini University of Naples \u201cFederico II,\u201d Naples, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Germano","family":"Guerra","sequence":"additional","affiliation":[{"name":"Department of Health Sciences, University of Molise, Via F. 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