Spatiotemporal expression of three gap junction gene products involved in fetomaternal communication during rat pregnancy

Development ◽  
1991 ◽  
Vol 113 (1) ◽  
pp. 165-181 ◽  
Author(s):  
B. Risek ◽  
N.B. Gilula

The expression of three different members of the gap junction multigene family, alpha 1 (Cx43), beta 1 (Cx32), and beta 2 (Cx26), was analysed in the rat implantation chamber (a structural unit containing fetal, extraembryonic and maternal components within the pregnant uterus) during mid- and late stages of gestation as well as in the delivering, post-partum and non-pregnant uterus. A differential, spatiotemporal and cell-type-specific regulation of gap junctional coexpression was observed for beta 1 and beta 2 in all epithelia examined (visceral, luminal and glandular), as well as for alpha 1 and beta 2 in decidual cells and keratinocytes of the fetal epidermis. alpha 1 antigen was detected in the mesometrial stroma, mesometrial myometrium, connective tissue, mesothelia of the amnion and visceral yolk sac and in the allantoic mesodermal layer throughout gestation. In addition, expression of alpha 1 in the placental basal zone and trophoblast giant cells coincided with the differentiation of these cells. beta 2 expression was observed prominently in the chorionic villi of the placental labyrinth. The presence of beta 1 and beta 2 in the visceral epithelium (visceral yolk sac = the primary route for embryonic nourishment prior to the formation of the chorioallantoic placenta) and beta 2 in the chorionic villi (placental barrier = the major fetomaternal exchange route) suggests that gap junctions have an important role in fetomaternal communication.

Development ◽  
1985 ◽  
Vol 86 (1) ◽  
pp. 125-141
Author(s):  
I. Damjanov ◽  
A. Damjanov ◽  
P. W. Andrews

The retransplantable tumour line derived from a spontaneous ovarian murine teratocarcinoma (Fekete & Ferigno, 1952) was cloned and characterized using light and electron microscopic and immunohistochemical techniques. Grown in ascites, the tumour consisted predominantly of stem cells and a small number of differentiated derivatives. The stem cells expressed surface reactivity with antibody to SSEA-3 and Forssman antigen, alkaline phosphatase, focal cytoplasmic reactivity with antibody to SSEA-1, and varying amounts of cytoplasmic glycogen and 3 betahydroxysteroid dehydrogenase. Their cytoskeleton reacted with antibodies to keratin and vimentin. The differentiated derivatives formed approximately 5–15% of the total cell population in ascites and appeared either as giant cells or were characterized by their reactivity with antibodies to H-2 or α-foetoprotein or intracellular and pericellular laminin or high levels of 3 betahydroxysteroid dehydrogenase activity. Solid tumours produced from subcutaneously injected cells had a variegated appearance suggesting, that like the limited differentiation in the ascites, the stem cells can give rise to trophoblastic, as well as parietal and visceral yolk sac elements. On the basis of the presented data the tumour stem cells were considered as representing malignant equivalents of the common precursor of trophoblastic, visceral and parietal yolk sac cells most likely corresponding to trophectoderm. Accordingly, the tumour was designated as trophectodermal carcinoma.


Author(s):  
William P. Jollie

A technique has been developed for visualizing antibody against horseradish peroxidase (HRP) in rat visceral yolk sac, the placental membrane across which passive immunity previously has been shown to be transferred from mother to young just prior to birth. Female rats were immunized by injecting both hind foot pads with 1 mg HRP emulsified in complete Freund's adjuvant. They were given a booster of 0.5mg HRP in 0.1 ml normal saline i.v. after one week, then bred and autopsied at selected stages of pregnancy, viz., 12, 1 7 and 22 days post coitum, receiving a second booster, injected as above, five days before autopsy. Yolk sacs were removed surgically and fixed immediately in 2% paraformaldehye, 1% glutaraldehye in 0.1 M phosphate buffer with 0.01% CaCl2 at pH 7.4, room temperature, for 3 hr, rinsed 3X in 0.1 M phosphate buffer plus 5% sucrose, then exposed to 1 mg HRP in 1 ml 0.1 M phosphate buffer at pH 7.4 for 1 hr. They were refixed in aldehydes, as above, for 1 5 min (to assure binding of antigen-antibody complex). Following buffer washes, the tissues were incubated in 3 mg diaminobenzidine tetrahydrochloride and 0.01% H2O2 in 0.05 M Tris-HCl buffer for 30 min. After brief buffer washes, they were postfixed in 2% OsO4. in phosphate buffer at pH 7.4, 4°C for 2 hr, dehydrated through a graded series of ethanols, and embedded in Durcupan. Thin sections were observed and photographed without contrast-enhancement with heavy metals. Cytochemical reaction product marked the site of HRP (i.e., antigen) which, in turn, was present only where it was bound with anti-HRP antibody.


Viruses ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 554
Author(s):  
Natália Salomão ◽  
Michelle Brendolin ◽  
Kíssila Rabelo ◽  
Mayumi Wakimoto ◽  
Ana Maria de Filippis ◽  
...  

Intrauterine transmission of the Chikungunya virus (CHIKV) during early pregnancy has rarely been reported, although vertical transmission has been observed in newborns. Here, we report four cases of spontaneous abortion in women who became infected with CHIKV between the 11th and 17th weeks of pregnancy. Laboratorial confirmation of the infection was conducted by RT-PCR on a urine sample for one case, and the other three were by detection of IgM anti-CHIKV antibodies. Hematoxylin and eosin (H&E) staining and an electron microscopy assay allowed us to find histopathological, such as inflammatory infiltrate in the decidua and chorionic villi, as well as areas of calcification, edema and the deposition of fibrinoid material, and ultrastructural changes, such as mitochondria with fewer cristae and ruptured membranes, endoplasmic reticulum with dilated cisterns, dispersed chromatin in the nuclei and the presence of an apoptotic body in case 1. In addition, by immunohistochemistry (IHC), we found a positivity for the anti-CHIKV antibody in cells of the endometrial glands, decidual cells, syncytiotrophoblasts, cytotrophoblasts, Hofbauer cells and decidual macrophages. Electron microscopy also helped in identifying virus-like particles in the aborted material with a diameter of 40–50 nm, which was consistent with the size of CHIKV particles in the literature. Our findings in this study suggest early maternal fetal transmission, adding more evidence on the role of CHIKV in fetal death.


1960 ◽  
Vol 11 (3) ◽  
pp. 365 ◽  
Author(s):  
CW Stump ◽  
JP Robins ◽  
ML Garde

The material consists of 20 embryos (5-30 mm) and two foetuses (63 mm and 90 mm) collected at whaling stations on Moreton and Norfolk Islands (latitude 27� 11'S. and 29� 5' S. respectively) during late August, September, and early October in 1952-53-54 and 1956. The consecutive series permitted the study of membrane formation and organogenesis. Younger embryos are found in grooves between the folds of endometrium in a constant site in that uterine horn associated with the ovary containing the recent corpus luteum. Older embryos and the early foetus are adapted to lie freely in the uterine fluid, and are devoid of any mechanism for apposition or attachment to the endometrium. Variation in the sequence of the association of the components of the umbilical cord provides suspensory structures for the amnion and yolk sac, and for the embryo a bifid ligament, retained in the early foetus for attachment of the foetal membranes. In the younger foetus the allantoic duct drains the nephric secretion into the uterine cavity. In the older foetus chorionic villi are present. The bifid suspensory ligament forms the major part of the distal region of the umbilical cord. The allantoic duct is reunited with the allantoic sac. Amniogenesis is by folding. During the embryonic period the chorio-amniotic connection forms a suspensory ligament. The yolk sac, attached by a novel ligament to the amnion, is large and functional in the embryo. In the foetus vascular splanchnopleure is present in a tubular form. A rete system develops in the embryo.


Placenta ◽  
1991 ◽  
Vol 12 (2) ◽  
pp. 143-151 ◽  
Author(s):  
John D. Grubb ◽  
Thomas R. Koszalk ◽  
Joseph J. Drabick ◽  
Robert M. Metrione

Development ◽  
1972 ◽  
Vol 27 (3) ◽  
pp. 543-553
Author(s):  
D. A. T. New ◽  
R. L. Brent

Rat embryos, explanted with their embryonic membranes during the early stages of organogenesis ( days gestation), were grown in culture in roller tubes. Yolk-sac antibody (sheep anti rat yolk-sac gamma globulin), known to be teratogenic when injected into pregnant rats, was added to the culture medium. At concentrations of 0·1 mg/ml or more the antibody caused gross retardation of growth and differentiation. Injection of antibody into the amniotic cavity so that it had direct contact with the embryo, or between the amnion and yolk sac so that it was in contact with the mesodermal surface of the yolk sac, had little or no effect on development of the embryo or its membranes. These in vitro experiments indicate that yolk-sac antibody has an effect on development independent of any immunological reaction of the mother, and the primary action is probably on the visceral yolk-sac endoderm.


Development ◽  
1964 ◽  
Vol 12 (1) ◽  
pp. 1-14
Author(s):  
Aeleta N. Barber ◽  
Jack C. Geer

Since the discovery of the teratogenicity of trypan blue by Gillman, Gilbert, Gilhnan and Spence (1948) the dye has offered a very concise and convenient method for studying teratogenesis in mammals. Dijkstra & Gillman (1960) fractionated the dye and found that the purple component stimulated the endothelial system in rats, thereby raising the speculation that the varied effects of the dye were caused by contamination. According to our previous experiments (1957, 1963) and those of Wilson, Beaudoin & Free (1959) one aspect of the problem has remained fairly constant, namely, the narrow time limit of the maximal effect of the dye and the stability of the pattern of malformations. Wilson and his associates suggest that the teratogenic effect is due to direct access of the dye to the embryo before the visceral yolk-sac is completely formed.


Mitochondrion ◽  
2008 ◽  
Vol 8 (5-6) ◽  
pp. 389-395 ◽  
Author(s):  
M.P. Alcolea ◽  
B. Colom ◽  
E. Amengual-Cladera ◽  
I. Lladó ◽  
M. Gianotti ◽  
...  
Keyword(s):  
Yolk Sac ◽  

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