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The growth of new blood vessels (a process known as angiogenesis) is essential during embryonic development, wound healing, and blood cell development in the bone marrow, but it also has a role in supporting tumor growth. It is a finely tuned process regulated by a balance of pro- and anti-angiogenic factors, and in a study appearing in the December issue of the Journal of Clinical Investigation, researchers from Weill Medical College, New York, show that in mice, two types of blood cell (known as megakaryocytes and platelets) produce antiangiogenic factors known as thrombospondins. Using mice lacking both thrombospondin 1 and thrombospondin 2, Shahin Rafii and colleagues showed that the production of these factors limits the angiogenesis that supports blood cell development in the bone marrow after treatment with chemotherapeutic drugs. These factors also limited the blood vessel growth that accompanies wound healing in response to a loss of blood flow in the tissues. The increased blood vessel growth in these situations was mediated by increased activation of a protein known as MMP9 and by increased production of a proangiogenic factor known as SDF1. This study has clinical implications because inhibiting the release of thromobospondins by megakaryocytes and platelets might provide a new approach to enhance blood vessel growth (and thereby restore blood cell development) after chemotherapy. In an accompanying commentary, Judith Varner, from the Moores UCSD (University of California, San Diego) Cancer Center, discusses how the identification of these antiangiogenic factors furthers our understanding of the finely regulated process of angiogenesis, and highlights some of the questions that remain to be answered. TITLE: Thrombospondins deployed by thrombopoietic cells determine angiogenic switch and extent of revascularization AUTHOR CONTACT: Shahin Rafii Weill Medical College of Cornell University, New York, New York, USA.
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