Effect of Mer overexpression on HMEC-1 cell angiogenesis and its mechanism.
- Author:
Lei FAN
1
;
Meng-Yun ZHOU
;
Fei SHEN
;
Li-Qian XIE
;
Chang-Geng RUAN
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line; Cell Movement; Cell Proliferation; Endothelial Cells; metabolism; physiology; Endothelium, Vascular; cytology; Humans; 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
- From: Chinese Journal of Hematology 2007;28(9):602-604
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore anti-angiogenesis effect of Mer, a member of tyrosine kinase receptor family, and its mechanism.
METHODSHuman 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.
RESULTSAfter 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.
CONCLUSIONOverexpressed Mer tyrosine kinase receptor can inhibit the migration and angiogenesis of HMEC-1 cells through VEGF-C/VEGFR-2 signal pathway.
