Results
| PMID | 23334337 |
| Gene Name | VEGFC |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 15 |
| Population details | 15 (10 peritoneal endometriosis, 5 controls) |
| Age | 26–42 yrs |
| Sex | Female |
| Infertility type | Female infertility |
| Associated genes | VEGF-A, VEGF-B, VEGF-C |
| Other associated phenotypes |
Angiogenesis in endometriosis |
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Angiogenesis. 2013 Jul;16(3):541-51. doi: 10.1007/s10456-013-9333-1. Epub 2013 Xu, Hui| Zhang, Tao| Man, Gene Chi Wai| May, Katie E| Becker, Christian M| Davis, Tina N| Kung, Andrew L| Birsner, Amy E| D'Amato, Robert J| Wong, Alice Wai Yee| Wang, Chi Chiu Department of Obstetrics and Gynaecology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong. Endometriosis is an angiogenesis-dependent disease. Many studies demonstrated inhibition of angiogenesis leads to inhibition of endometriotic growth, however underlying mechanism is still not fully understood. Our previous study suggested vascular endothelial growth factor C (VEGF-C) as a target of anti-angiogenesis therapy for endometriosis. In this study, VEGF-C in endometrium and its role in angiogenesis of endometriosis were studied. Human endometrium were obtained from women with and without endometriosis for molecular studies. VEGF-A, VEGF-B, VEGF-C and VEGF-D mRNA and proteins in eutopic and ectopic endometrium were measured. Human endothelial cells were transfected with VEGF-C siRNA in vitro, effects of VEGF-C on endothelial cell migration, invasion and tube formation were investigated in vitro. Angiogenesis was inhibited in wild type mice, vascular permeability in dermal skin was determined in vivo. Transplanted endometrium were inhibited by VEGF-C siRNA in immunocompromised mice, development, growth and angiogenesis of the experimental endometriosis were compared in vivo. The results showed that VEGF-C mRNA and protein were increased in eutopic and ectopic endometrium of endometriosis patients. VEGF-C siRNA significantly inhibited endothelial cell migration and tube formation. VEGF-C siRNA significantly inhibited development and angiogenesis of the experimental endometriotic lesions in mice. Supplementation and over-expression of VEGF-C significantly reversed the inhibitory effects on the endothelial functions, vascular permeability and endometriotic growth. In conclusion, VEGF-C is increased in endometrium and it promotes endothelial functions, vascular permeability and development of experimental endometriosis. VEGF-C is important for angiogenesis in endometriosis. Mesh Terms: Analysis of Variance| Animals| Capillary Permeability/*physiology| Cell Movement/drug effects/physiology| Endometriosis/*metabolism| Endometrium/cytology/*metabolism| Endothelial Cells/metabolism/*physiology| Female| Humans| Mice| Neovasculariza |
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