Regulation of trophoblast beta1-integrin expression by contact with endothelial cells
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Regulation of trophoblast beta1-integrin expression by contact with endothelial cells Twanda L Thirkill1, Sonia R Hendren1, Arlen Soghomonians2, Natalie F Mariano1, Abdul I Barakat2 and Gordon C Douglas*1 Address: 1Department of Cell Biology and Human Anatomy, School of Medicine, University of California, Davis CA 95616, USA and 2Department of Mechanical and Aeronautical Engineering, University of California, Davis CA 95616, USA Email: Twanda L Thirkill - [email protected]; Sonia R Hendren - [email protected]; Arlen Soghomonians - [email protected]; Natalie F Mariano - [email protected]; Abdul I Barakat - [email protected]; Gordon C Douglas* - [email protected] * Corresponding author
Published: 09 June 2004 Cell Communication and Signaling 2004, 2:4
Received: 09 March 2004 Accepted: 09 June 2004
This article is available from: http://www.biosignaling.com/content/2/1/4 © 2004 Thirkill et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
Abstract Background: In human and non-human primates, migratory trophoblasts penetrate the uterine epithelium, invade uterine matrix, and enter the uterine vasculature. Invasive trophoblasts show increased expression of β1 integrin. Since trophoblast migration within the uterine vasculature involves trophoblast attachment to endothelial cells lining the vessel walls, this raises the possibility that cell-cell contact and/or factors released by endothelial cells could regulate trophoblast integrin expression. To test this, we used an in vitro system consisting of early gestation macaque trophoblasts co-cultured on top of uterine microvascular endothelial cells. Results: When cultured alone, trophoblasts expressed low levels of β1 integrin as determined by quantitative immunofluorescence microscopy. When trophoblasts were cultured on top of endothelial cells for 24 h, the expression of trophoblast β1 integrin was significantly increased as determined by image analysis. β1 Integrin expression was not increased when trophoblasts were cultured with endothelial cell-conditioned medium, suggesting that upregulation requires direct contact between trophoblasts and endothelial cells. To identify endothelial cell surface molecules responsible for induction of trophoblast integrin expression, trophoblasts were cultured in dishes coated with recombinant platelet endothelial cell adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1), or αVβ3 integrin. Trophoblast β1 integrin expression (assessed by immunofluorescence microscopy and Western blotting) was increased when PECAM-1 or αVβ3 integrin, but not ICAM-1, was used as substrate. Conclusions: Direct contact between trophoblasts and endothelial cells increases the expression of trophoblast β1 integrin.
Background As part of the implantation process and development of the pla
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