scholarly journals MRI analysis of angiogenesis during mouse embryo implantation

2006 ◽  
Vol 55 (5) ◽  
pp. 1013-1022 ◽  
Author(s):  
Vicki Plaks ◽  
Vyacheslav Kalchenko ◽  
Nava Dekel ◽  
Michal Neeman
Keyword(s):  
Mouse Embryo ◽  
Embryo Implantation

2-Methoxyoestradiol impairs mouse embryo implantation via F-spondin

2019 ◽  
Vol 31 (4) ◽  
pp. 689
Author(s):  
Emanuel Guajardo-Correa ◽  
Denisse Mena-Silva ◽  
Patricia Diaz ◽  
Carlos Godoy-Guzmán ◽  
Hugo Cardenas ◽  
...  
Keyword(s):  
Mouse Embryo ◽  
Embryo Implantation ◽  
Target Protein ◽  
Methyl Transferase ◽  
Uterine Fluid ◽  
Protein F

The anti-implantation effects of high oestradiol (E2) concentrations could be mediated by E2 metabolites. Herein, we examined whether 2-methoxyoestradiol (2ME) impairs embryo implantation via its target protein F-spondin. Mice on Day 3 of pregnancy were treated with E2 concomitantly with the cathecol-O-methyl transferase inhibitor OR486 and the number of implanted embryos was recorded 5 days later. The effect of 2ME or 4-methoxyoestradiol (4ME) on embryo implantation was also investigated. Plasma and uterine levels of 2ME were measured 0.5, 1 or 3h after E2 treatment while the mRNA for spondin 1 (Spon1) and F-spondin were determined in the uterus 3, 6, 12 or 24h after 2ME treatment. Finally, the effect of a neutralising F-spondin antibody on the anti-implantation effect of 2ME was explored. OR486 blocked the anti-implantation effect of E2; 2ME, but not 4ME, affected embryo implantation. The 2ME concentration was increased after 0.5 and 1h in plasma and 3h in uterine fluid following E2 treatment. 2ME increased levels of Spon1 at 12 and 24h although F-spondin was increased at 12h. F-spondin antibody blocked the effect of 2ME on embryo implantation. We conclude that 2ME impairs mouse embryo implantation via activation of F-spondin in the uterus.

scholarly journals Effect of 32/67 kDa laminin-binding protein antibody on mouse embryo implantation

Reproduction ◽  
2000 ◽  
Vol 119 (1) ◽  
pp. 137-142 ◽  
Author(s):  
C Zhang ◽  
E Duan ◽  
Y Cao ◽  
G Jiang ◽  
G Zeng
Keyword(s):  
Mouse Embryo ◽  
Binding Protein ◽  
Embryo Implantation ◽  
Laminin Binding Protein ◽  
Laminin Binding

scholarly journals Progesterone-regulated Hsd11b2 as a barrier to balance mouse uterine corticosterone

2020 ◽  
Vol 244 (1) ◽  
pp. 177-187 ◽  
Author(s):  
Hong-Tao Zheng ◽  
Tao Fu ◽  
Hai-Yi Zhang ◽  
Zhen-Shan Yang ◽  
Zhan-Hong Zheng ◽  
...  
Keyword(s):  
Early Pregnancy ◽  
Mouse Embryo ◽  
Stromal Cells ◽  
Inner Cell Mass ◽  
Local Level ◽  
Embryo Implantation ◽  
Cell Mass ◽  
Type I ◽  
Mouse Uterus ◽  
Ovariectomized Mice

Glucocorticoids (GCs) are essential for mouse embryo implantation and decidualization. Excess GCs are harmful for mouse embryo implantation and decidualization. 11β-Hydroxysteroid dehydrogenases type I and II (Hsd11b1/Hsd11b2) are main enzymes for regulating local level of GCs. Hsd11b2 acts as the placental glucocorticoid barrier to protect the fetus from excessive exposure. Although effects of GCs on the fetus and placenta in late pregnancy have been extensively studied, the effects of these adrenal corticosteroids in early pregnancy are far less well defined. Therefore, we examined the expression, regulation and function of Hsd11b1/Hsd11b2 in mouse uterus during early pregnancy. We found that Hsd11b2 is highly expressed in endometrial stromal cells on days 3 and 4 of pregnancy and mainly upregulated by progesterone (P4). In both ovariectomized mice and cultured stromal cells, P4 significantly stimulates Hsd11b2 expression. P4 stimulation of Hsd11b2 is mainly mediated by the Ihh pathway. The uterine level of corticosterone (Cort) is regulated by Hsd11b2 during preimplantation. Embryo development and the number of inner cell mass cells are suppressed by Cort treatment. These results indicate that P4 should provide a low Cort environment for the development of preimplantation mouse embryos by promoting the expression of uterine Hsd11b2.

The expression and function of cystatin C and cathepsin B and cathepsin L during mouse embryo implantation and placentation

Development ◽  
1997 ◽  
Vol 124 (17) ◽  
pp. 3415-3425
Author(s):  
S. Afonso ◽  
L. Romagnano ◽  
B. Babiarz
Keyword(s):  
Cystatin C ◽  
Mouse Embryo ◽  
Cathepsin B ◽  
Proteinase Inhibitors ◽  
Cathepsin L ◽  
Embryo Implantation ◽  
Giant Cells ◽  
Major Product ◽  
Normal Embryo ◽  
And Function

The implantation of the mouse embryo requires the controlled invasion of the uterine stroma by the embryonic trophoblast. This event is dependent, in part, on the secretion of matrix metalloproteinases and serine proteinases for the extracellular degradation of the uterine matrix. Proteinase activity is controlled by stromal decidualization and specific proteinase inhibitors. This work adds to our understanding of implantation and placentation by reporting the expression and function of another class of proteinases/inhibitors closely related to invasive cell behavior. We focused on the cysteine proteinases, cathepsins B and L, and their inhibitor cystatin C. Northern blots showed that trophoblast expressed cathepsin B throughout the invasive period (days 5.5-10.5). Both cathepsin B message and cathepsin L protein were localized to the mature, invasive trophoblast giant cells. Substrate gel electrophoresis showed an increase in giant cell cathepsin activity with enzyme profiles changing at the end of the invasive period. Northern and western blotting showed that cystatin C, the main inhibitor of cathepsins, was a major product of the decidualizing stroma. Message levels first increased in peripheral decidualizing cells, with the protein localizing close to the embryo during implantation (days 5.5-8.5). With the regression of the decidua beginning on day 9.5, a coordinated upregulation of both cathepsin B and cystatin C was observed implying a role for controlled cathepsin expression during apoptosis. E-64, a synthetic inhibitor of cathepsins B and L, was injected into pregnant females at the stage of blastocyst attachment (days 4.5-5.5). High doses resulted in the complete failure of implantation while lower doses resulted in stunted embryos and a reduced decidual reaction. These results suggested that cathepsins B and L are necessary for normal embryo development and uterine decidualization, and that decidua contributes to their control by a coordinated expression of cystatin C within the implantation site.

Effect of 32/67 kDa laminin-binding protein antibody on mouse embryo implantation

Reproduction ◽  
2000 ◽  
pp. 137-142 ◽  
Author(s):  
C Zhang ◽  
E Duan ◽  
Y Cao ◽  
G Jiang ◽  
G Zeng
Keyword(s):  
Extracellular Matrix ◽  
Mouse Embryo ◽  
Binding Protein ◽  
Embryo Implantation ◽  
Continuous Section ◽  
Rabbit Igg ◽  
Laminin Binding Protein ◽  
Ectoplacental Cone ◽  
Laminin Binding

Mouse embryo implantation depends on the complex interaction between the embryo trophoblast cells and the uterine environment, which deposits an extracellular matrix with abundant amounts of laminin. Intrauterine injection and blastocyst or ectoplacental cone culture models were used to study the effect of 32/67 kDa laminin-binding protein antibody on mouse embryo implantation in vivo and in vitro. Intrauterine injection of 32/67 kDa laminin-binding protein antibody (0.4 mg in 1 ml Ham's F-10 medium, 5 microl per mouse) into the left uterine horns of mice (n = 22) on day 3 of pregnancy inhibited embryo implantation significantly (P < 0.001) compared with the contralateral horns that had been injected with normal rabbit IgG. A continuous section study on day 5 after injection showed that the embryos in the control uteri implanted normally and developed healthily, but there were no embryos or the remaining embryos had disintegrated in the uteri injected with 32/67 kDa laminin-binding protein antibody. Blastocysts or ectoplacental cones were cultured in media containing 32/67 kDa laminin-binding protein antibody (0.2 mg ml(-1)) on laminin-coated dishes with normal rabbit IgG at the same concentration as in the controls. The 32/67 kDa laminin-binding protein had no effect on blastocyst or ectoplacental cone attachment, but prohibited the blastocyst or ectoplacental cone outgrowth and primary or secondary trophoblast giant cell migration. These results indicate that 32/67 kDa laminin-binding protein antibody blocked mouse embryo implantation by preventing embryo trophoblast cell invasion and migration through the uterine decidual basement membrane-like extracellular matrix which has a high laminin content.

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