scholarly journals Galectin-9: A New Endometrial Epithelial Marker for the Mid- and Late-Secretory and Decidual Phases in Humans

2005 ◽  
Vol 90 (11) ◽  
pp. 6170-6176 ◽  
Author(s):  
Roxana M. Popovici ◽  
Miriam S. Krause ◽  
Ariane Germeyer ◽  
Thomas Strowitzki ◽  
Michael von Wolff

Abstract Context: The galectin family has been reported to play a role in the regulation of cell growth, cell adhesion, apoptosis, inflammation, and immunomodulation, all of which are important for endometrial function, as well as implantation. Objective: The objective of the study was to investigate the expression and regulation of galectin-9, a β-galactoside-binding lectin in the human endometrium. Design: Galectin-9 mRNA and protein were analyzed in dated endometrial biopsies throughout the menstrual cycle and in human early-pregnancy decidua, as well as in the different endometrial cell compartments. Regulation of galectin-9 by estradiol, progesterone, epidermal growth factor, and interferon-γ in endometrial epithelial cells in vitro was studied. Results: Galectin-9 mRNA analyzed by RNase protection assay is expressed in the human endometrium, specifically in the human endometrial epithelial cells but not in stromal or immune cells. It is expressed at very low concentrations during the proliferative phase and the early-secretory phase and shows a sharp and significant increase in the mid- and late-secretory phases, the window of implantation, as well as in the decidua. Accordingly, galectin-9 protein is also exclusively increased in human endometrial epithelial cells during the mid- and late-secretory phases and in the decidua, however, not in endometrial stromal cells or decidualized cells in vivo or in vitro. A regulation in vitro by estradiol, progesterone, epidermal growth factor, and interferon-γ could not be detected. Conclusions: Based on these findings and on the functional studies of other galectins, we suggest galectin-9 as a novel endometrial marker for the mid- and late-secretory and decidual phases.

1995 ◽  
Vol 133 (6) ◽  
pp. 741-746 ◽  
Author(s):  
Toshifumi Machida ◽  
Michiyoshi Taga ◽  
Hiroshi Minaguchi

Machida T, Taga M, Minaguchi H. Effects of epidermal growth factor and transforming growth factor alpha on the mouse trophoblast outgrowth in vitro. Eur J Endocrinol 1995;133:741–6. ISSN 0804–4643 In order to analyze the involvement of growth factors in the implantation mechanism, we examined the direct effects of epidermal growth factor (EGF) and transforming growth factor alpha (TGF-α) on trophoblast outgrowth of the mouse blastocyst in vitro. ICR mouse blastocysts were cultured for 4 days on a culture plate in medium containing EGF or TGF-α or conditioned medium obtained from cultured endometrial epithelial cells. Blastocysts were also co-cultured with endometrial epithelial cells. The trophoblast outgrowth of these cultured blastocysts was observed daily and the percentage of outgrowing embryos was calculated and analyzed statistically by the chi-squared test. Analysis for the specific binding of 125I-EGF in outgrown trophoblasts was carried out by autoradiography. The coculture (days 3 and 4) and the presence of EGF (10 ng/ml, day 4), TGF-α (1 ng/ml, day 3; 10 ng/ml, days 2 and 3; 50 ng/ml, days 2–4) or conditioned medium (days 3 and 4) significantly stimulated the rate of trophoblast outgrowth. Preincubation of the conditioned medium with monoclonal anti-EGF or anti-TGF-α antibody suppressed the stimulatory effect of the conditioned medium on trophoblast outgrowth. The specific 125I-EGF binding in outgrown trophoblasts was demonstrated by autoradiography. These results suggest that EGF and TGF-α play an important role in the implantation process by directly stimulating trophoblast development. Michiyoshi Taga, Department of Obstetrics and Gynecology, Yokohama City University School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236, Japan


2010 ◽  
Vol 299 (3) ◽  
pp. G614-G622 ◽  
Author(s):  
Andrew A. Maynard ◽  
Katerina Dvorak ◽  
Ludmila Khailova ◽  
Holly Dobrenen ◽  
Kelly M. Arganbright ◽  
...  

Necrotizing enterocolitis (NEC) is a devastating intestinal disease of premature infants. Epidermal growth factor (EGF) is one of the most promising candidates in NEC prophylaxis. Autophagy regulates cell homeostasis, but uncontrolled activation of autophagy may lead to cellular injury. The aim was to evaluate the effects of EGF on intestinal autophagy in epithelial cells and in the rat NEC model and measure autophagy in NEC patients. Intestinal epithelial cells (IEC-6) and the rat NEC model were used to study the effect of EGF on intestinal autophagy. Protein levels of Beclin 1 and LC3II were measured in the intestinal epithelium in both in vivo and in vitro models. Ultrastructural changes in intestinal epithelium were studied by electron microscopy. Expression of Beclin 1, LC3II, and p62 protein was evaluated in biopsies from NEC patients. Autophagy was induced in IEC-6 cells and inhibited by adding EGF into the culture. In the rat NEC model, EGF treatment of NEC reduced expression of Beclin 1 and LC3II in ileal epithelium. Morphologically, typical signs of autophagy were observed in the epithelium of the NEC group, but not in the EGF group. A strong signal for Beclin 1 and LC3II was detected in the intestine from patients with NEC. Autophagy is activated in the intestinal epithelium of NEC patients and in the ileum of NEC rats. Supplementation of EGF blocks intestinal autophagy in both in vivo and in vitro conditions. Results from this study indicate that EGF-mediated protection against NEC injury is associated with regulation of intestinal autophagy.


Nephron ◽  
1994 ◽  
Vol 68 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Makoto Kawaguchi ◽  
Fumie Kawashima ◽  
Keisuke Ohshima ◽  
Satoru Kawaguchi ◽  
Hiroyoshi Wada

1981 ◽  
Vol 90 (2) ◽  
pp. 537-541 ◽  
Author(s):  
J Keski-Oja ◽  
V P Lehto ◽  
I Virtanen

The effects of epidermal growth factor (EGF) on the cytokeratin filaments of cultured murine epithelial cells were studied by the indirect immunofluorescence technique with affinity-purified antibodies. Mouse epithelial cells (MMC-E), grown on glass cover slips, and viewed by immunofluorescence microscopy, showed keratin-specific fluorescence as typical bright perinuclear aggregates corresponding to dense paracrystalline granules seen in electron microscopy. Within minutes after an exposure to EGF, the keratin granules in the MMC-E cells decreased. After 10 min of incubation, the cells had spread fibrillar keratin. Such an effect could not be found after a similar exposure to insulin, dexamethasone, dibutyryl cyclic AMP, or antimitotic drugs. EGF, therefore, has a relatively direct effect on the cytoskeletal organization of cultured epithelial cells. These rapid effects on the keratin filaments may explain the simultaneous EGF-induced ultrastructural surface changes of the cells. EGF may thus function as a regulatory factor in the migration of epithelial cells and in the mobility of their cell membranes. The epithelial cell line, MMC-E, should prove a useful model for studies on the action of EGF on nontransformed epithelial cells in vitro.


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