The Regulators of VEGF Expression in Mouse Ovaries.
10.3349/ymj.2005.46.5.679
- Author:
So Young SHIN
1
;
Ho Jung LEE
;
Duck Sung KO
;
Hoi Chang LEE
;
Won Il PARK
Author Information
1. Department of Obstetrics & Gynecology, Eulji University School of Medicine, Seoul, Korea. pwi3110@eulji.or.kr
- Publication Type:Original Article
- Keywords:
Angiogenesis inducing agents;
follicle stimulating hormone;
interleukin-6;
ovary;
vascular endothelial growth factors
- MeSH:
Vascular Endothelial Growth Factor A/analysis/*genetics;
RNA, Messenger/analysis;
Ovary/*metabolism;
Mice, Inbred ICR;
Mice;
Interleukin-6/pharmacology;
Immunohistochemistry;
Gene Expression Regulation/*drug effects;
Follicle Stimulating Hormone/pharmacology;
Female;
Chorionic Gonadotropin/pharmacology;
Antigens, CD34/analysis;
Animals
- From:Yonsei Medical Journal
2005;46(5):679-686
- CountryRepublic of Korea
- Language:English
-
Abstract:
The objectives of this study were to explore whether ovarian vascular endothelial growth factor (VEGF) expression in mice can be regulated by IL-6 (interleukin-6), angiotensin II, FSH, and hCG; and to test whether the mouse ovarian VEGF expression can result in angiogenesis. The ICR mice were sacrificed, and their ovaries were recovered. Recovered ovaries were treated with IL-6, angiotensin II, FSH, and hCG separately and incubated for 24 hours in alpha-MEM. Expression of mRNA and protein of VEGF were assessed by RT-PCR and immunohistochemistry. The resulting angiogenesis was evaluated through immunohistochemical analysis for CD34. Treatment of mice ovaries with IL-6, FSH, and hCG resulted in a significant increase of VEGF mRNA, and IL-6 was the most potent inducer of VEGF. IL-6 and FSH resulted in increased neovascularization in the follicular phase of mouse ovaries. In contrast, angiotensin II could not increase VEGF expression or neovascularization. We documented an in vitro increase in VEGF expression by IL-6, FSH, and hCG; and reaffirmed that the proliferative response of murine ovarian endothelial cells paralleled an increase of VEGF expression.