Molecular Human Reproduction, Vol. 6, No. 3, 269-275,
March 2000
© 2000 European Society of Human Reproduction and Embryology
Uterine physiology |
Induction of an angiogenic phenotype in endometriotic stromal cell cultures by interleukin-1ß
1 Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, HSE 1689, Box 0556, San Francisco, CA 94143–0556, and 2 Division of Immunology, Genentech Inc, South San Francisco, CA 94080–4990, USA
Abstract
Activated peritoneal macrophages are associated with endometriosis and may play a central role in its aetiology by releasing interleukin-1ß (IL-1ß) in response to refluxed endometrium. Pari passu with the establishment of endometriotic implants is the development of a vascular supply. In this study we investigated the angiogenic properties of two endometrial proteins, vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6), and assessed their production in response to IL-1ß stimulation in human stromal cells isolated from normal endometrium (NE) and endometriotic lesions (EI). Proliferation of bovine brain capillary endothelial cells (BBCE) with a [3H]-thymidine incorporation assay was observed when VEGF (2.1 ± 0.2-fold; P < 0.05) or VEGF and IL-6 (1.8 ± 0.1-fold; P < 0.05) were added in vitro, relative to saline-treated control cultures. Northern blot analysis showed induction of VEGF mRNA (2.6-fold; P < 0.05) and IL-6 mRNA (6.3-fold; P < 0.05) transcripts in EI cells, but not NE cells, exposed to IL-1ß. A similar induction was seen with VEGF and IL-6 protein secretion in the responsive EI cells. Reverse transcription–polymerase chain reaction (RT–PCR) for the IL-1 receptor type I (IL-1 RI) indicated that the differential effects of IL-1ß on NE and EI cells was associated with 2.4 ± 0.1-fold more receptor mRNA in EI versus NE cells. We propose that the ability of IL-1ß to activate an angiogenic phenotype in EI stromal cells but not in NE cells, is mediated by the IL-1 RI.
angiogenesis factor/cytokines/endometriosis/interleukin-1/neovascularization
Notes
3 To whom correspondence should be addressed
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