The gonadotropins: Tissue-specific angiogenic factors?

被引:63
作者
Reisinger, K.
Baal, N.
McKinnon, T.
Minstedt, K.
Zygmunt, M.
机构
[1] Univ Giessen, Dept Obstet & Gynecol, D-35385 Giessen, Germany
[2] EMA Univ Greifswald, Dept Obstet & Gynecol, D-17475 Greifswald, Germany
关键词
gonadotropins; hCG; angiogenesis; female reproductive organs;
D O I
10.1016/j.mce.2006.11.015
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The gonadotropins, whose members are human chorionic gonadotropin (hCG), lutenizing hormone (LH) and follicle-stimulating hormone (FSH) are a well characterized hormone family known to regulate reproductive functions in both females and males. Recent studies indicate that they can modulate the vascular system of reproductive organs. It was shown that gonadotropins not only influence the expression of vascular endothelial growth factor (VEGF) and both its receptors VEGFR-1 and -2, but also modulate other ubiquitously expressed angiogenic factors like the angiopoietins and their receptor Tie-2, basic fibroblast growth factor or placental-derived growth factor. Some recent data indicates a possible direct action of gonadotropins on endothelial cells. Thus, the gonadotropins act as tissue-specific angiogenic factors providing an optimal vascular supply during the menstrual cycle and early pregnancy in the female reproductive tract as well as in testis. In pathological conditions (e.g. preeclampsia, intrauterine growth restriction, ovarian hyperstimulation or endometriosis), these tightly regulated interactions between the gonadotropins and the ubiquitous angiogenic factors appear to be disturbed. The intent of this short manuscript is to review the current knowledge of the regulatory role of the gonadotropins in vasculo- and angiogenesis. We also review angiogenic actions of thyroid-stimulating hormone (TSH), a glycoprotein closely related to gonadotropins, which display strong gonodal actions. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:65 / 80
页数:16
相关论文
共 221 条
[61]   Expression, production, and secretion of vascular endothelial growth factor and interleukin-6 by granulosa cells is comparable in women with and without endometriosis [J].
Garrido, N ;
Albert, C ;
Krüssel, JS ;
O'Connor, JE ;
Remohí, J ;
Simón, C ;
Pellicer, A .
FERTILITY AND STERILITY, 2001, 76 (03) :568-575
[62]   EFFECTS OF MULTIPLE INJECTIONS OF HCG ON TESTIS BLOOD-FLOW [J].
GEESAMAN, B ;
VILLANUEVAMEYER, J ;
BLUESTEIN, D ;
MILLER, L ;
MENA, I ;
RAJFER, J .
UROLOGY, 1992, 40 (01) :81-83
[63]   Uncovering molecular mechanisms involved in activation of G protein-coupled receptors [J].
Gether, U .
ENDOCRINE REVIEWS, 2000, 21 (01) :90-113
[64]   Human placental vascular development: Vasculogenic and angiogenic (branching and nonbranching) transformation is regulated by vascular endothelial growth factor-A, angiopoietin-1, and angiopoietin-2 [J].
Geva, E ;
Ginzinger, DG ;
Zaloudek, CJ ;
Moore, DH ;
Byrne, A ;
Jaffe, RB .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (09) :4213-4224
[65]   Role of vascular endothelial growth factor in ovarian physiology and pathology [J].
Geva, E ;
Jaffe, RB .
FERTILITY AND STERILITY, 2000, 74 (03) :429-438
[66]   FETAL UMBILICAL ARTERY FLOW VELOCITY-TIME WAVEFORMS IN TWIN PREGNANCIES [J].
GILES, WB ;
TRUDINGER, BJ ;
COOK, CM .
BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY, 1985, 92 (05) :490-497
[67]  
Goede V, 1998, LAB INVEST, V78, P1385
[68]   Administration of low-dose LH induces ovulation and prevents vascular hyperpermeability and vascular endothelial growth factor expression in superovulated rats [J].
Gómez, R ;
Lima, I ;
Simón, C ;
Pellicer, A .
REPRODUCTION, 2004, 127 (04) :483-489
[69]   Administration of moderate and high doses of gonadotropins to female rats increases ovarian vascular endothelial growth factor (VEGF) and VEGF receptor-2 expression that is associated to vascular hyperpermeability [J].
Gömez, R ;
Simón, C ;
Remohí, J ;
Pellicer, A .
BIOLOGY OF REPRODUCTION, 2003, 68 (06) :2164-2171
[70]   Vascular endothelial growth factor receptor-2 activation induces vascular permeability in hyperstimulated rats, and this effect is prevented by receptor blockade [J].
Gómez, R ;
Simón, C ;
Remohí, J ;
Pellicer, A .
ENDOCRINOLOGY, 2002, 143 (11) :4339-4348