| Summary: | 碩士 === 臺北醫學大學 === 醫學科學研究所 === 97 === 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. It has been known that several growth factors and cytokines were released during angiogenesis, such as VEGF and IL-1 beta. The aim of this thesis study is to examine the molecular mechanisms underlying IL-1 beta-induced human umbilical vein endothelial cells migration inhibition. To gain this purpose, we treated HUVEC with IL-1 beta. Our data demonstrated that after 24 hours IL-1 beta treatment up-regulated the expression of Thy-1 mRNA and protein, activated PKC delta and inhibited HUVEC migration and capillary-like tube formation. Moreover, we found that treatment of HUVEC with PKC delta inhibitor, Röttlerin, dramatically reversed the IL-1 beta-induced inhibition of cell migration and tube formation. Knockdown Thy-1 protein by transfection of Thy-1 siRNA into HUVEC partially reversed the IL-1 beta-induced inhibition of cell migration. Taken together, our data suggest that IL-1 betanmight induce migration inhibition in HUVEC though up-regulation of Thy-1 molecule via a PCK delta-dependent pathway.
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