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Chinese Journal of Hematology ; (12): 602-604, 2007.
Article in Chinese | WPRIM | ID: wpr-262976

ABSTRACT

<p><b>OBJECTIVE</b>To explore anti-angiogenesis effect of Mer, a member of tyrosine kinase receptor family, and its mechanism.</p><p><b>METHODS</b>Human Mer full length plasmid was transfected into HMEC-1 cells through liposome. G418 was used to select positive clone. Expression of Mer at mRNA and protein level was detected by real-time PCR and Western-blot, respectively. Transwell and Matrigel were used to evaluate the effect of overexpressed Mer on migration and angiogenesis of HMEC-1 cells. Primary angiogenesis associated factor VEGF-A, VEGF-B, VEGF-C, VEGF-D and VEGFR-1, VEGFR-2 were screened by real-time PCR.</p><p><b>RESULTS</b>After G418 selection, the Mer expression in transfected HMEC-1 cells was increased 3.61- and 2.12 fold at mRNA and protein level, respectively. Compared with negative control, the migration of Mer-HMEC-1 was decreased (21 +/- 6 vs 36 +/- 11), and angiogenesis capability on Matrigel significantly decreased. By real-time PCR, the expression of VEGF-C and VEGFR-2 was down-regulated to 44.7% and 25.6% of the negative control.</p><p><b>CONCLUSION</b>Overexpressed Mer tyrosine kinase receptor can inhibit the migration and angiogenesis of HMEC-1 cells through VEGF-C/VEGFR-2 signal pathway.</p>


Subject(s)
Humans , Cell Line , Cell Movement , Cell Proliferation , Endothelial Cells , Metabolism , Physiology , Endothelium, Vascular , Cell Biology , Neovascularization, Physiologic , Proto-Oncogene Proteins , Genetics , Metabolism , RNA, Messenger , Metabolism , Receptor Protein-Tyrosine Kinases , Genetics , Metabolism , Receptors, Vascular Endothelial Growth Factor , Metabolism , Transfection , Vascular Endothelial Growth Factors , Metabolism , c-Mer Tyrosine Kinase
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