Effect of Mer overexpression on HMEC-1 cell angiogenesis and its mechanism

• Published in: Zhōnghuá xuèyèxué zázhì Vol. 28; no. 9; p. 602
• Main Authors: Fan, Lei, Zhou, Meng-Yun, Shen, Fei, Xie, Li-Qian, Ruan, Chang-Geng
• Format: Journal Article
• Language: Chinese
• Published: China 01.09.2007
• Subjects: c-Mer Tyrosine Kinase; Cell Line; Cell Movement; Cell Proliferation; Endothelial Cells - metabolism; Endothelial Cells - physiology; Endothelium, Vascular - cytology; Humans; Neovascularization, Physiologic; Proto-Oncogene Proteins - genetics; Proto-Oncogene Proteins - metabolism; Receptor Protein-Tyrosine Kinases - genetics; Receptor Protein-Tyrosine Kinases - metabolism; Receptors, Vascular Endothelial Growth Factor - metabolism; RNA, Messenger - metabolism; Transfection; Vascular Endothelial Growth Factors - metabolism
• ISSN: 0253-2727

To explore anti-angiogenesis effect of Mer, a member of tyrosine kinase receptor family, and its mechanism. 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. 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. Overexpressed M