DEMONSTRATION OF THE LOW-AFFINITY ALPHA-SUBUNIT OF THE GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR-RECEPTOR (GM-CSF-R-ALPHA) ON HUMAN TROPHOBLAST AND UTERINE CELLS

Citation
Pp. Jokhi et al., DEMONSTRATION OF THE LOW-AFFINITY ALPHA-SUBUNIT OF THE GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR-RECEPTOR (GM-CSF-R-ALPHA) ON HUMAN TROPHOBLAST AND UTERINE CELLS, Journal of reproductive immunology, 26(2), 1994, pp. 147-164
Citations number
42
Categorie Soggetti
Reproductive Biology",Immunology
ISSN journal
01650378
Volume
26
Issue
2
Year of publication
1994
Pages
147 - 164
Database
ISI
SICI code
0165-0378(1994)26:2<147:DOTLAO>2.0.ZU;2-0
Abstract
Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a classic al haematopoietic cytokine which has also been implicated in placental growth and development. In this study we have performed a detailed im munohistological localization of the low affinity GM-CSF receptor (GM- CSF-R alpha) in human first trimester implantation site and non-pregna nt endometrium, We have also investigated receptor expression and GM-C SF binding in vitro by normal first trimester trophoblast using flow c ytometric analysis and compared this with JEG-3 and JAR choriocarcinom a cells. In the first trimester, the GM-CSF-R was found to be present on villous cytotrophoblast and all populations of extravillous trophob last. Expression by villous syncytiotrophoblast was weak or absent, bu t this increased markedly by term. GM-CSF-R were also expressed by fet al Hofbauer cells within the mesenchyme of the chorionic villi and by uterine glandular epithelium and decidual macrophages within maternal decidua. GM-CSF-R was not expressed by glands in proliferative phase e ndometrium but began to appear during the secretory phase, suggesting hormonal regulation of the receptor on uterine glandular epithelium. F low cytometric comparison of normal isolated first trimester trophobla st and JEG-3 and JAR choriocarcinoma cells revealed two- to threefold higher surface expression of GM-CSF-R by choriocarcinoma cells and hig her binding capacity for rhGM-CSF than normal trophoblast. These resul ts suggest that GM-CSF may regulate growth and development of human tr ophoblast. GM-CSF may also influence placental development and functio n by acting via decidual and fetal macrophages, and uterine glandular epithelium, which are the other cell populations to express the recept or.