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 Blood, 15 February 2008, Vol. 111, No. 4, pp. 1980-1988.
Prepublished online as a Blood First Edition Paper on November 27, 2007; DOI 10.1182/blood-2007-06-094680.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

{alpha}2β1 integrin expression in the tumor microenvironment enhances tumor angiogenesis in a tumor cell–specific manner

Zhonghua Zhang1, Norma E. Ramirez1, Thomas E. Yankeelov2,5, Zhengzhi Li1, Laura E. Ford1, Ying Qi1, Ambra Pozzi6,7, and Mary M. Zutter1,7

1 Department of Pathology, 2 Department of Radiology and Radiological Sciences, 3 Department of Biomedical Engineering, 4 Department of Physics and Astronomy, 5 Institute of Imaging Science, 6 Department of Medicine, and 7 Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN

To define the role of the {alpha}2β1 integrin in pathologic angiogenesis, we investigated tumor-associated growth and angiogenesis in wild-type and {alpha}2-null mice. Our findings reveal that the {alpha}2β1 integrin plays an important role in angiogenesis via regulation of VEGFR1 expression. When challenged with B16F10 melanoma cells, mice lacking {alpha}2β1 integrin ex-pression exhibit increased tumor angiogenesis associated with up-regulated VEGFR1 expression. In contrast, there was no {alpha}2β1 integrin-dependent difference in the angiogenic response to Lewis lung carcinoma (LLC) cells. Interestingly, whereas B16F10 cells secrete high levels of placental growth factor (PLGF), LLC cells produce high levels of VEGF, but low levels of PLGF. The {alpha}2β1 integrin-dependent difference in angiogenesis was restored to LLC cells by expression of PLGF, strongly suggesting that the angiogenic phenotype and tumor growth in the {alpha}2-null host is dependent on specific interactions between the tumor cell and the genetically defined integrin repertoire of the host microenvironment. Thus integrin {alpha}2-null mice represent an example of genetic alterations of "the soil" determining response to the "seed."


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