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At least 217 records · Page 12Linked to original sources
PubMed2000

Early pregnancy factor activity in serum of patients with surgical abortion.

PROBLEM: The presence of early pregnancy factor (EPF) has been repeatedly confirmed as indispensable to successful pregnancy. However, there is as yet little reported about how surgical abortion would affect the EPF activity, owing to the induced embryo loss. The aim of this study was to pursue this among a large number of patients available in the People's Republic of China. METHOD: Sera from aborters were collected before surgical abortion and again on the 3rd, 5th and 7th day after treatment. EPF activity was detected by rosette inhibition assay. RESULTS: Before surgical abortion, the mean level of EPF in pregnancy sera was about the same as that of the positive control. After surgical abortion, the EPF level declined rapidly for the first 3 days and then dropped gradually within the negative control range after 5-7 days. DISCUSSION: Quantitative study of EPF activity along temporal dimensions (duration) due to surgical abortion further promotes the efficiency to take EPF activity and its rate of change as truly index for monitoring embryonic care and development of normal pregnancy.

Abortion, Induced↗
PubMed2001

Epigenetic instability in ES cells and cloned mice.

Cloning by nuclear transfer (NT) is an inefficient process in which most clones die before birth and survivors often display growth abnormalities. In an effort to correlate gene expression with survival and fetal overgrowth, we have examined imprinted gene expression in both mice cloned by nuclear transfer and in the embryonic stem (ES) cell donor populations from which they were derived. The epigenetic state of the ES cell genome was found to be extremely unstable. Similarly, variation in imprinted gene expression was observed in most cloned mice, even in those derived from ES cells of the same subclone. Many of the animals survived to adulthood despite widespread gene dysregulation, indicating that mammalian development may be rather tolerant to epigenetic aberrations of the genome. These data imply that even apparently normal cloned animals may have subtle abnormalities in gene expression.

Animals↗
PubMed2004

Rescue of cardiac defects in id knockout embryos by injection of embryonic stem cells.

We report that Id knockout mouse embryos display multiple cardiac defects, but mid-gestation lethality is rescued by the injection of 15 wild-type embryonic stem (ES) cells into mutant blastocysts. Myocardial markers altered in Id mutant cells are restored to normal throughout the chimeric myocardium. Intraperitoneal injection of ES cells into female mice before conception also partially rescues the cardiac phenotype with no incorporation of ES cells. Insulin-like growth factor 1, a long-range secreted factor, in combination with WNT5a, a locally secreted factor, likely account for complete reversion of the cardiac phenotype. Thus, ES cells have the potential to reverse congenital defects through Id-dependent local and long-range effects in a mammalian embryo.

Animals↗
PubMed1998

Purification and expression of the Tf190 adhesin in Tritrichomonas foetus.

Bovine trichomoniasis is a sexually transmitted disease caused by Tritrichomonas foetus and characterized by early embryo loss. The mechanism of this loss is not known, although the parasite is known to cause inflammation and to have the ability to kill host cells by a contact-dependent cytotoxic mechanism. Antibody specific for a 190,000-Da surface complex (Tf190) was previously shown to inhibit this adhesion. In this study we used immunoaffinity chromatography to purify Tf190 from T. foetus in order to analyze its composition and examine its expression. Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of purified Tf190 followed by silver staining revealed three components of Tf190. Western blotting and antibody-binding experiments showed that the 140- and 60-kDa bands were immunogenic. By using a battery of monoclonal antibodies (MAbs) periodate-sensitive epitopes were identified on Tf190, suggesting that these epitopes contained carbohydrate structures. Analyses of affinity-purified Tf190 by high-performance liquid chromatography and gas-liquid chromatography demonstrated the presence of the monosaccharides and lipids known to be prominent constituents of the lipophosphoglycan (LPG) of T. foetus. Flow cytometry experiments on several isolates of T. foetus with Tf190-specific antibodies revealed that Tf190 was present on subpopulations of all isolates but that not all epitopes were present on every isolate. This pattern of reactivities on the different parasite isolates was confirmed by Western blots of whole-parasite extracts probed with MAbs and antiserum. These results suggest that although variation in the expression of epitopes of Tf190 occurs in different strains of T. foetus, the Tf190 adhesion complex is widespread in different populations of the parasite. The data further suggest that immunogenic structures, important in the adhesion of T. foetus to mammalian cells, are located in the LPG-like component of Tf190.

Animals↗
PubMed2001

The mouse snail gene encodes a key regulator of the epithelial-mesenchymal transition.

Snail family genes encode DNA binding zinc finger proteins that act as transcriptional repressors. Mouse embryos deficient for the Snail (Sna) gene exhibit defects in the formation of the mesoderm germ layer. In Sna(-/-) mutant embryos, a mesoderm layer forms and mesodermal marker genes are induced but the mutant mesoderm is morphologically abnormal. Lacunae form within the mesoderm layer of the mutant embryos, and cells lining these lacunae retain epithelial characteristics. These cells resemble a columnar epithelium and have apical-basal polarity, with microvilli along the apical surface and intercellular electron-dense adhesive junctions that resemble adherens junctions. E-cadherin expression is retained in the mesoderm of the Sna(-/-) embryos. These defects are strikingly similar to the gastrulation defects observed in snail-deficient Drosophila embryos, suggesting that the mechanism of repression of E-cadherin transcription by Snail family proteins may have been present in the metazoan ancestor of the arthropod and mammalian lineages.

Abnormalities, Multiple↗
PubMed2002

Activating transcription factor 1 and CREB are important for cell survival during early mouse development.

Activating transcription factor 1 (ATF1), CREB, and the cyclic AMP (cAMP) response element modulatory protein (CREM), which constitute a subfamily of the basic leucine zipper transcription factors, activate gene expression by binding as homo- or heterodimers to the cAMP response element in regulatory regions of target genes. To investigate the function of ATF1 in vivo, we inactivated the corresponding gene by homologous recombination. In contrast to CREB-deficient mice, which suffer from perinatal lethality, mice lacking ATF1 do not exhibit any discernible phenotypic abnormalities. Since ATF1 and CREB but not CREM are strongly coexpressed during early mouse development, we generated mice deficient for both CREB and ATF1. ATF1(-/-) CREB(-/-) embryos die before implantation due to developmental arrest. ATF1(+/-) CREB(-/-) embryos display a phenotype of embryonic lethality around embryonic day 9.5 due to massive apoptosis. These results indicate that CREB and ATF1 act in concert to mediate signals essential for maintaining cell viability during early embryonic development.

Activating Transcription Factor 1↗
PubMed2002

Involvement of mouse Rev3 in tolerance of endogenous and exogenous DNA damage.

The Rev3 gene of Saccharomyces cerevisiae encodes the catalytic subunit of DNA polymerase zeta that is implicated in mutagenic translesion synthesis of damaged DNA. To investigate the function of its mouse homologue, we have generated mouse embryonic stem cells and mice carrying a targeted disruption of Rev3. Although some strain-dependent variation was observed, Rev3(-/-) embryos died around midgestation, displaying retarded growth in the absence of consistent developmental abnormalities. Rev3(-/-) cell lines could not be established, indicating a cell-autonomous requirement of Rev3 for long-term viability. Histochemical analysis of Rev3(-/-) embryos did not reveal aberrant replication or cellular proliferation but demonstrated massive apoptosis in all embryonic lineages. Although increased levels of p53 are detected in Rev3(-/-) embryos, the embryonic phenotype was not rescued by the absence of p53. A significant increase in double-stranded DNA breaks as well as chromatid and chromosome aberrations was observed in cells from Rev3(-/-) embryos. The inner cell mass of cultured Rev3(-/-) blastocysts dies of a delayed apoptotic response after exposure to a low dose of N-acetoxy-2-acetylaminofluorene. These combined data are compatible with a model in which, in the absence of polymerase zeta, double-stranded DNA breaks accumulate at sites of unreplicated DNA damage, eliciting a p53-independent apoptotic response. Together, these data are consistent with involvement of polymerase zeta in translesion synthesis of endogenously and exogenously induced DNA lesions.

Acetoxyacetylaminofluorene↗
PubMed2004

Placental failure and impaired vasculogenesis result in embryonic lethality for neuropathy target esterase-deficient mice.

Age-dependent neurodegeneration resulting from widespread apoptosis of neurons and glia characterize the Drosophila Swiss Cheese (SWS) mutant. Neuropathy target esterase (NTE), the vertebrate homologue of SWS, reacts with organophosphates which initiate a syndrome of axonal degeneration. NTE is expressed in neurons and a variety of nonneuronal cell types in adults and fetal mice. To investigate the physiological functions of NTE, we inactivated its gene by targeted mutagenesis in embryonic stem cells. Heterozygous NTE(+/-) mice displayed a 50% reduction in NTE activity but underwent normal organ development. Complete inactivation of the NTE gene resulted in embryonic lethality, which became evident after gastrulation at embryonic day 9 postcoitum (E9). As early as E7.5, mutant embryos revealed growth retardation which did not reflect impaired cell proliferation but rather resulted from failed placental development; as a consequence, massive apoptosis within the developing embryo preceded its resorption. Histological analysis indicated that NTE is essential for the formation of the labyrinth layer and survival and differentiation of secondary giant cells. Additionally, impairment of vasculogenesis in the yolk sacs and embryos of null mutant conceptuses suggested that NTE is also required for normal blood vessel development.

Alleles↗
PubMed2005

The reaper-binding protein scythe modulates apoptosis and proliferation during mammalian development.

Scythe (BAT3 [HLA-B-associated transcript 3]) is a nuclear protein that has been implicated in apoptosis, as it can modulate Reaper, a central apoptotic regulator in Drosophila melanogaster. While Scythe can markedly affect Reaper-dependent apoptosis in Xenopus laevis cell extracts, the function of Scythe in mammals is unknown. Here, we report that inactivation of Scythe in the mouse results in lethality associated with pronounced developmental defects in the lung, kidney, and brain. In all cases, these developmental defects were associated with dysregulation of apoptosis and cellular proliferation. Scythe-/- cells were also more resistant to apoptosis induced by menadione and thapsigargin. These data show that Scythe is critical for viability and normal development, probably via regulation of programmed cell death and cellular proliferation.

Animals↗
PubMed2005

Dosage-dependent effects of Akt1/protein kinase Balpha (PKBalpha) and Akt3/PKBgamma on thymus, skin, and cardiovascular and nervous system development in mice.

Akt/protein kinase B (PKB) plays a critical role in the regulation of metabolism, transcription, cell migration, cell cycle progression, and cell survival. The existence of viable knockout mice for each of the three isoforms suggests functional redundancy. We generated mice with combined mutant alleles of Akt1 and Akt3 to study their effects on mouse development. Here we show that Akt1-/- Akt3+/- mice display multiple defects in the thymus, heart, and skin and die within several days after birth, while Akt1+/- Akt3-/- mice survive normally. Double knockout (Akt1-/-) Akt3-/-) causes embryonic lethality at around embryonic days 11 and 12, with more severe developmental defects in the cardiovascular and nervous systems. Increased apoptosis was found in the developing brain of double mutant embryos. These data indicate that the Akt1 gene is more essential than Akt3 for embryonic development and survival but that both are required for embryo development. Our results indicate isoform-specific and dosage-dependent effects of Akt on animal survival and development.

Animals↗
PubMed1985

A cytogenetic study of subfertility in the domestic cat (Felis catus).

The chromosomes of cat embryos derived from three subfertile queens were studied 4 weeks postcoitum. The incidence of spontaneous chromosome anomalies was 15% and type of abnormality observed was autosomal mosaicism. The significance of this finding and the developmental fate of the chromosomally aberrant embryos is discussed. The absence of polyploidy and (nonmosaic) autosomal trisomy, which are the most common observations in previous studies on mammalian embryos, suggests that the difference between the present observations and previous studies may be related to the difference in gestational stage studied, or to the difference in ovulatory patterns between domestic cats and other mammals. Polyploidy through ageing of the gametes is less likely in the cat than in spontaneous ovulators since ovulation in cats is induced only after coitus. It is speculated that chromosome analysis of earlier stages of embryonic development may reveal more severe forms of karyotype alteration.

Animals↗
PubMed2005

The influence of dehydroepiandrosterone on early pregnancy in mice.

The aim of the present report was to study the role of high levels of dehydroepiandrosterone (DHEA) on the ovarian function and embryonic resorption during early pregnancy in BALB/c mice. Pregnant animals were injected with DHEA following both the post-implantatory (DHEA-2) and peri-implantatory (DHEA-6) models. Morphological studies of implantation sites showed 40% of embryonic resorption in the DHEA-2 group while 100% of resorption was observed in the DHEA-6 group. Serum samples of both DHEA-2 and DHEA-6 groups showed higher estradiol levels and a lower progesterone concentration than those of control groups. Ovarian prostaglandin E levels after both DHEA-2 and DHEA-6 treatments increased when compared to control groups. The antioxidant metabolite glutathione diminished during both DHEA treatments. In summary, the data presented here suggest that DHEA treatment during early pregnancy modulates the ovarian function and is responsible for embryonic resorption with different degrees depending on when it is administered.

Adjuvants, Immunologic↗
PubMed1979

Pinealectomy-induced changes in blood and pituitary luteinizing and prolactin levels during the last phase of pregnancy in rats.

Serum LH levels were higher in pinealectomized than in sham-operated control rats during all 4 of the last days of pregnancy studied, although reaching significance only during the final 2 days, 21 and 22. Prolactin (Prl) levels in the serum on the final day of pregnancy, and its contents in the pituitary throughout the entire study period, were significantly lower in pinealectomized rats. Pituitary weights were lower in pinealectomized than in control animals during days 21 and 22 of pregnancy, but no differences were found between the 2 groups in the average number of living foetuses and resorptions. The results presented would seem to indicate that during the last phase of pregnancy the pineal gland plays a role in the modification of gonadotropin synthesis and release. It appears that with LH the release, and with Prl mainly the synthesis, is being affected by the pineal, although the release of Prl may be influenced as well.

Animals↗