scholarly journals BMP7 coordinates endometrial epithelial cell receptivity for blastocyst implantation through the endoglin pathway in cell lines and a mouse model

Author(s):  
Caixia Yuan ◽  
Xianlian Li ◽  
Haixia Song ◽  
Lingling Fan ◽  
Shili Su ◽  
...  
2010 ◽  
Vol 84 (1) ◽  
pp. 41-51 ◽  
Author(s):  
Wedad Aboussahoud ◽  
Reza Aflatoonian ◽  
Chris Bruce ◽  
Sarah Elliott ◽  
Jon Ward ◽  
...  

2000 ◽  
Vol 24 (1) ◽  
pp. 135-144 ◽  
Author(s):  
B Husen ◽  
N Psonka ◽  
M Jacob-Meisel ◽  
C Keil ◽  
GM Rune

In the endometrium two enzymes are known to convert estradiol to its inactive metabolite estrone: microsomal 17beta-hydroxysteroid dehydrogenase type 2 (17beta-HSD2) and peroxisomal 17beta-HSD4. In order to elucidate the particular function of each of these two different enzymes, the human endometrial epithelial cell lines HEC-1-A and RL95-2 were examined with respect to the expression of 17betaHSD isozymes. They were compared with human endometrium in vivo. Non-radioactive in situ hybridization revealed both enzymes in glandular epithelial cells of human endometrium. The two cell lines were screened for mRNA expression of 17beta-HSD 1-4 by RT-PCR and Northern blot. 17beta-HSD2 and 4 could be detected by either method, 17beta-HSD1 only by RT-PCR, 17beta-HSD3 not at all. Both cell lines were proven to have no receptor for progesterone which is known as a physiological inducer of several 17beta-HSD isozymes. To study the regulation of 17beta-HSD2 and 17betaHSD4, the concentration of fetal calf serum in the cell culture media was reduced stepwise to 0.3% by dilution with a defined serum replacement. This treatment led to an inhibition of 17beta-HSD2 mRNA expression and an increase in the mRNA expression of 17beta-HSD4. Concomitantly, distinct morphological changes were observed, such as a decrease in the number and length of microvilli and a decrease in the formation of domes on top of the monolayers. The endometrial epithelial cell lines HEC-1-A and RL95-2 represent a suitable in vitro model for further studies of the differential expression of the major endometrial HSD isozymes, independent of the effect of progesterone.


2014 ◽  
Vol 81 (4) ◽  
pp. 326-340 ◽  
Author(s):  
Sonali R. Bhagwat ◽  
Tejashree Redij ◽  
Kruttika Phalnikar ◽  
Sumeet Nayak ◽  
Swati Iyer ◽  
...  

Reproduction ◽  
2006 ◽  
Vol 131 (4) ◽  
pp. 733-742 ◽  
Author(s):  
A W Horne ◽  
E-N Lalani ◽  
R A Margara ◽  
J O White

Oestrogen, progesterone and paracrine signals from the embryo have been associated with the overall control of implantation. Changes in the expression of the heavily glycosylated transmembrane glycoprotein MUC1 mucin on the endometrial epithelium are also thought to be important for embryo attachment. Increased MUC1 expression has been correlated with elevated progesterone levels in the secretory phase of the menstrual cycle. Embryonic control of endometrial receptivity through changes in MUC1 expression could be achieved through the interleukin-1 system. Four endometrial epithelial cell lines (HEC1A, HEC1B, Ishikawa and RL592) were treated with oestrogen and progesterone (with or without interleukin-1-beta) and were subjected to immunocytochemistry and flow cytometric analysis to determine MUC1 production using MUC1 antibodies. HEC1A (oestrogen receptor (ER) and progesterone receptor (PR) positive) and HEC1B (ER positive and PR negative) were transfected with theMUC1promoter, underwent similar treatment regimes and the activity of theMUC1promoter relative to their untreated controls was determined using a chloramphenicol acetyltransferase (CAT) enzyme-linked immunoassay. Using the cell lines, we determined that endometrial MUC1 expression is up-regulated by progesterone, consistent with thein vivoincreases in MUC1 related to high progesterone levels. We also revealed that neither oestrogen, nor interleukin-1-beta, appear to modulate MUC1. Progesterone-dependent regulation of MUC1 is likely to be an important factor in determining endometrial receptivity.


1990 ◽  
Vol 26 (12) ◽  
pp. 1173-1179 ◽  
Author(s):  
S. Tabibzadeh ◽  
K. L. Kaffka ◽  
P. L. Kilian ◽  
P. G. Satyaswaroop

1999 ◽  
Vol 67 (7) ◽  
pp. 3625-3630 ◽  
Author(s):  
James C. Comolli ◽  
Alan R. Hauser ◽  
Leslie Waite ◽  
Cynthia B. Whitchurch ◽  
John S. Mattick ◽  
...  

ABSTRACT Type IV pili of the opportunistic pathogen Pseudomonas aeruginosa mediate twitching motility and act as receptors for bacteriophage infection. They are also important bacterial adhesins, and nonpiliated mutants of P. aeruginosa have been shown to cause less epithelial cell damage in vitro and have decreased virulence in animal models. This finding raises the question as to whether the reduction in cytotoxicity and virulence of nonpiliated P. aeruginosa mutants are primarily due to defects in cell adhesion or loss of twitching motility, or both. This work describes the role of PilT and PilU, putative nucleotide-binding proteins involved in pili function, in mediating epithelial cell injury in vitro and virulence in vivo. Mutants of pilT and pilU retain surface pili but have lost twitching motility. In three different epithelial cell lines, pilT or pilU mutants of the strain PAK caused less cytotoxicity than the wild-type strain but more than isogenic, nonpiliated pilA or rpoN mutants. ThepilT and pilU mutants also showed reduced association with these same epithelial cell lines compared both to the wild type, and surprisingly, to a pilA mutant. In a mouse model of acute pneumonia, the pilT and pilUmutants showed decreased colonization of the liver but not of the lung relative to the parental strain, though they exhibited no change in the ability to cause mortality. These results demonstrate that pilus function mediated by PilT and PilU is required for in vitro adherence and cytotoxicity toward epithelial cells and is important in virulence in vivo.


2015 ◽  
Vol 20 (3) ◽  
pp. 399-409 ◽  
Author(s):  
Xiangguo Wang ◽  
Pengfei Lin ◽  
Yanlong Yin ◽  
Jinhua Zhou ◽  
Lanjie Lei ◽  
...  

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