Lipocortin-1 is modulated by glucocorticoids in the human endometrium
AD Taylor1, KJ Bedford1, J Robinson2, I Richmond3, S Maguiness3, IP Adams1 & SL Atkin1
Lipocortin 1 (LC1) is a well-characterized anti-inflammatory, -anti mitotic and anti-proliferative member of a structurally related family of Ca2+ and phospholipid-binding proteins. LC1 is readily detectable in the neuroendocrine system by Western blot analysis, ELISA, and immunohistochemistry (1). In these tissues, glucocorticoids regulate both the expression and subcellular distribution of LC1. Other studies have also demonstrated the presence of LC1 in endometrium tissue though the exact role is not known. In the present study we have used established methods (1) to investigate the presence of LC1 in normal endometrial tissue biopsies collected from patients undergoing mock embryo transfer and investigated the effects of glucocorticoids on the cellular distribution. Tissue was collected at day 21 of their cycle and incubated for 1-4h under controlled conditions. Where appropriate dexamethasone (Dex), progesterone, oestrogen and testosterone (0.1nM-0.1micromolar) were included throughout the experiment. Pericellular and intracellular LC1 were detected by SDS-PAGE and Western blot analysis (1). Western analysis demonstrated the presence of ir-LC1 37kDa within the pericellular and extracellular regions of the endometrial tissue. The amount of ir-LC1 within the pericellular pool increased with time and reached a maximum at 2.5h. This effect was paralleled with a concomitant decrease in the intracellular LC1. In response to incubation of the tissue with Dex there was an increase in the ir-LC1 pericellular pool, which was maximal at 100nM; again these observations were paralleled with a concomitant decrease in the intracellular LC1. In a parallel set of experiments Ishikawa cells (an immortalised differentiated endometrium cell line) demonstrated a parallel profile of data. In all cases progesterone, testosterone and oestrogen were ineffective in this respect. In conclusion our data support the presence of LC1 within the endometrium throughout the menstrual cycle where its expression can be modulated by glucocorticoids.
1. Buckingham JC Int J Tissue React. 1998; 20(1):23-34.