| Summary: | 碩士 === 臺北醫學大學 === 細胞及分子生物研究所 === 95 === It has been recognized that angiogenesis is required in many physiological and pathological conditions. For instance, in the development of tumor, in order to get more nutrients, tumor cells promote vessel formation through the expression of angiogenic molecules in the microenvironment. The understanding that the growth of tumors depends on the acquisition of a blood supply has led to the development of new therapies strategy for cancer based on inhibition of angiogenesis. Previously, our laboratory has demonstrated that Thy-1 molecule was expressed in microvascular endothelial cells during angiogenesis and served as a marker for angiogenesis. The aim of this thesis study is to examine the roles of Thy-1 molecule during angiogenesis. To gain this purpose, we over-expressed Thy-1 protein by transfection of Thy-1 cDNA into HUVEC. Our data demonstrated that over-expression of Thy-1 did not affect the proliferation of endothelial cells, but inhibited the HUVEC migration, capillary-like tube formation, and down-regulated the Rho protein. Over-expression of Thy-1 did not affect the adhesion and viability of HUVEC, suggesting that Thy-1-induced inhibition of endothelial cell migration was not through altering the cell adhesion or the occurrence cell death. Moreover, we found that over-expression of RhoA V14 dramatically reversed the Thy-1-induced inhibition of cell migration and tube formation. However, pretreatment of the cells with ROCK inhibitor abolished the prevention effect of RhoA V14 on Thy-1-induced migration inhibition and tube formation. Taken together, these data suggest that Rho family might play an important role in the Thy-1-induced migration inhibition of HUVEC.
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