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Blood, 1 September 2006, Vol. 108, No. 5, pp. 1661-1667.
Prepublished online as a Blood First Edition Paper on May 9, 2006; DOI 10.1182/blood-2006-04-014563.
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NEOPLASIA
Loss of inhibitory semaphorin 3A (SEMA3A) autocrine loops in bone marrow endothelial cells of patients with multiple myeloma
Angelo Vacca,
Claudio Scavelli,
Guido Serini,
Giulia Di Pietro,
Teresa Cirulli,
Francesca Merchionne,
Domenico Ribatti,
Federico Bussolino,
Diego Guidolin,
Giovanna Piaggio,
Andrea Bacigalupo, and
Franco Dammacco
From the Department of Internal Medicine and Clinical Oncology and the Department of Human Anatomy and Histology, University of Bari Medical School, Bari; the Department of Oncological Sciences and Division of Molecular Angiogenesis, Institute for Cancer Research and Treatment, University of Turin Medical School, Candiolo; the Department of Human Anatomy and Physiology, University of Padua Medical School, Padua; and the Department of Hemato-Oncology, S Martino Hospital, Genoa, Italy.
Vascular endothelial growth factor165 (VEGF165) and semaphorin3A (SEMA3A) elicit pro- and antiangiogenic signals respectively in endothelial cells (ECs) by binding to their receptors VEGFR-2, neuropilin-1 (NRP1), and plexin-A1. Here we show that the VEGF165-driven angiogenic potential of multiple myeloma (MM) ECs is significantly higher than that of monoclonal gammopathy of undetermined significance (MGUS) ECs (MGECs) and human umbilical vein (HUV) ECs. This is probably due to a constitutive imbalance of endogenous VEGF165/SEMA3A ratio, which leans on VEGF165 in MMECs but on SEMA3A in MGECs and HUVECs. Exogenous VEGF165 induces SEMA3A expression in MGECs and HUVECs, but not in MMECs. Moreover, by counteracting VEGF165 activity as efficiently as an anti-VEGFR-2 antibody, exogenous SEMA3A restrains the over-angiogenic potential of MMECs. Our data indicate that loss of endothelial SEMA3A in favor of VEGF165 could be responsible for the angiogenic switch from MGUS to MM.
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