Modulation of alphafetoprotein synthesis in the early postimplantation mouse embryo

Development ◽  
1978 ◽  
Vol 46 (1) ◽  
pp. 135-146
Author(s):  
M. Dziadek

The visceral endoderm of mouse egg cylinders on the 7th and 8th days of gestation is divided into the visceral embryonic (VE) endoderm cell population which synthesizes alphafetoprotein (AFP), and the visceral extra-embryonic (VEX) endoderm population which does not synthesize AFP. Embryonic (E) and extra-embryonic (EX) ectoderm and visceral endoderm tissues were enzymically separated, reassociated in different combinations, and cultured in vitro for 48 h. The immunoperoxidase reaction on sections of cultured tissues showed that both VE and VEX endoderm cells synthesize high levels of AFP when cultured in isolation or in association with E ectoderm, but do not synthesize AFP when in close association with EX ectoderm. Both 7th and 8th day VEX endoderm cells synthesize detectable levels of AFP 12 h after isolation, and contain high levels by 24 h. It is concluded that both VE and VEX endoderm cells have the ability to synthesize AFP, but modulation of expression occurs through an inhibitory influence of the EX ectoderm.

Development ◽  
1981 ◽  
Vol 62 (1) ◽  
pp. 379-394
Author(s):  
Brigid L. M. Hogan ◽  
Rita Tilly

Morphological and biochemical evidence is presented that the visceral extraembryonic endoderm of the 6·5-day mouse embryo will differentiate into parietal endoderm when cultured in contact with extraembryonic ectoderm undergoing transition into trophoblast giant cells. Egg cylinders from 6·5-day embryos were dissected into embryonic and extraembryonic halves and cultured in suspension in vitro for up to 7 days. After 4 days, the endoderm cells of the extraembryonic fragments morphologically resemble parietal endoderm, are associated with a thick basement membrane and synthesize large amounts of the matrix proteins laminin and Type IV procollagen. A similar transition in phenotype is not seen in the endoderm of embryonic fragments, nor in visceral extraembryonic endoderm cells cultured in isolation. In another series of experiments, complete egg cylinders were dissected free of visceral endoderm ovei lying the extraembryonic ectoderm and then cultured in vitro. The visceral endoderm cells which recolonize the surface of the extraembryonic ectoderm develop a parietal endoderm phenotype and lay down a thick basement membrane. These results suggest that the differentiation of the extraembryonic endoderm of the early mouse embryo into visceral and parietal phenotypes can be influenced by local cell—cell or cell—substrate interactions, and is not determined solely by cell lineage.


Development ◽  
1981 ◽  
Vol 61 (1) ◽  
pp. 51-59
Author(s):  
Claude A. Cudennec ◽  
Gregory R. Johnson

Previous investigations have shown that the teratocarcinoma line PCC3/A/1 is able to differentiate in vitro to produce red blood cells of the primitive hemopoietic cell population of the mouse embryo. The present paper demonstrates the presence in the same cultures of multipotential cells capable of giving rise to colonies containing erythrocytes, macrophages, and megakaryocytes when stimulated by pokeweed-mitogen spleen-cell conditioned medium.


2020 ◽  
Vol 18 (2) ◽  
pp. 148-157 ◽  
Author(s):  
Triantafyllos Didangelos ◽  
Konstantinos Kantartzis

The cardiac effects of exogenously administered insulin for the treatment of diabetes (DM) have recently attracted much attention. In particular, it has been questioned whether insulin is the appropriate treatment for patients with type 2 diabetes mellitus and heart failure. While several old and some new studies suggested that insulin treatment has beneficial effects on the heart, recent observational studies indicate associations of insulin treatment with an increased risk of developing or worsening of pre-existing heart failure and higher mortality rates. However, there is actually little evidence that the associations of insulin administration with any adverse outcomes are causal. On the other hand, insulin clearly causes weight gain and may also cause serious episodes of hypoglycemia. Moreover, excess of insulin (hyperinsulinemia), as often seen with the use of injected insulin, seems to predispose to inflammation, hypertension, dyslipidemia, atherosclerosis, heart failure, and arrhythmias. Nevertheless, it should be stressed that most of the data concerning the effects of insulin on cardiac function derive from in vitro studies with isolated animal hearts. Therefore, the relevance of the findings of such studies for humans should be considered with caution. In the present review, we summarize the existing data about the potential positive and negative effects of insulin on the heart and attempt to answer the question whether any adverse effects of insulin or the consequences of hyperglycemia are more important and may provide a better explanation of the close association of DM with heart failure.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Pengfei Liu ◽  
Jing Yuan ◽  
Yetong Feng ◽  
Xin Chen ◽  
Guangsuo Wang ◽  
...  

AbstractFerroptosis is a novel type of programmed cell death, which is different from apoptosis and autophagic cell death. Recently, ferroptosis has been indicated to contribute to the in vitro neurotoxicity induced by isoflurane, which is one of the most common anesthetics in clinic. However, the in vivo position of ferroptosis in isoflurane-induced neurotoxicity as well as learning and memory impairment remains unclear. In this study, we mainly explored the relationship between ferroptosis and isoflurane-induced learning and memory, as well as the therapeutic methods in mouse model. Our results indicated that isoflurane induced the ferroptosis in a dose-dependent and time-dependent manner in hippocampus, the organ related with learning and memory ability. In addition, the activity of cytochrome c oxidase/Complex IV in mitochondrial electron transport chain (ETC) was increased by isoflurane, which might further contributed to cysteine deprivation-induced ferroptosis caused by isoflurane exposure. More importantly, isoflurane-induced ferroptosis could be rescued by both ferroptosis inhibitor (ferrostatin-1) and mitochondria activator (dimethyl fumarate), which also showed effective therapeutic action against isoflurane-induced learning and memory impairment. Taken together, our data indicate the close association among ferroptosis, mitochondria and isoflurane, and provide a novel insight into the therapy mode against isoflurane-induced learning and memory impairment.


1991 ◽  
Vol 29 (4) ◽  
pp. 265-274 ◽  
Author(s):  
T. Fujitani ◽  
M. Yoneyama ◽  
A. Ogata ◽  
T. Ueta ◽  
K. Mori ◽  
...  
Keyword(s):  

1994 ◽  
Vol 12 (1) ◽  
pp. 107-118 ◽  
Author(s):  
A Van Bael ◽  
R Huygen ◽  
B Himpens ◽  
C Denef

ABSTRACT We have studied the effect of LHRH and neuropeptide Y (NPY) on prolactin (PRL) mRNA levels in pituitary reaggregate cell cultures from 14-day-old female rats, by means of in situ hybridization and Northern blot analysis. As estimated by computer-image analysis, addition of LHRH on day 5 in culture for 40 h resulted in a 37% increase in the total cytoplasmic areas of cells containing PRL mRNA, visualized using a digoxigenin-labelled PRL cRNA. The size of individual PRL-expressing cells was not influenced, nor was the content of PRL mRNA per cell. A similar effect of LHRH was found by dot blot hybridization of extracted RNA. PRL mRNA levels were not affected by NPY. LHRH induced a 29% increase in the number of PRL mRNA-expressing cells processing through the S phase of the cell cycle, visualized by the incorporation of [3H]thymidine ([3H]T) into DNA over 16 h. The fraction of [3H]T-labelled cells was 10–12% of the total cell population. NPY did not influence the number of [3H]T-positive cells expressing PRL mRNA, but completely blocked the effect of LHRH on the latter population. The present data suggest that LHRH, probably via a paracrine action of gonadotrophs, stimulates the recruitment of new lactotrophs, an action which is negatively modulated by NPY. Since the magnitude of this effect was the same in the total pituitary cell population as in cells processing through the S phase of the cell cycle and presumably mitosis, recruitment of lactotrophs seems to be based on differentiation of progenitor or immature cells into PRL-expressing cells, rather than on a mitogenic action on pre-existing lactotrophs alone.


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