scholarly journals Effect of Bacterial Endotoxins on Superovulated Mouse Embryos In Vivo: Is CSF-1 Involved in Endotoxin-Induced Pregnancy Loss?

2006 ◽  
Vol 2006 ◽  
pp. 1-9 ◽  
Author(s):  
Yogesh Kumar Jaiswal ◽  
Madan Mohan Chaturvedi ◽  
Kaushik Deb
Keyword(s):  
Embryonic Development ◽  
Pregnancy Loss ◽  
Mouse Embryos ◽  
Preimplantation Embryos ◽  
Implantation Failure ◽  
Normal Pattern ◽  
Bacterial Endotoxins ◽  
Mammalian Embryonic Development ◽  
Lps Treatment

Mammalian embryonic development is regulated by several cytokines and growth factors from embryonic or maternal origins. Since CSF-1 plays important role in embryonic development and implantation, we investigated its role in gram-negative bacterial LPS-induced implantation failure. The effect of LPS on normal (nonsuperovulated) and superovulated in vivo-produced embryos was assessed by signs of morphological degeneration. A significantly similar number of morphologically degenerated embryos recovered from both nonsuperovulated and superovulated LPS treated animals on day 2.5 of pregnancy onwards were morphologically and developmentally abnormal as compared to their respective controls (P<.001. Normal CSF-1 expression level and pattern were also altered through the preimplantation period in the mouse embryos and uterine horns after LPS treatment. This deviation from the normal pattern and level of CSF-1 expression in the preimplantation embryos and uterine tissues suggest a role for CSF-1 in LPS-induced implantation failure.

Anti-silencing factor 1A is associated with genome stability maintenance of mouse preimplantation embryos†

2020 ◽  
Vol 102 (4) ◽  
pp. 817-827
Author(s):  
Kai Deng ◽  
Wanyou Feng ◽  
Xiaohua Liu ◽  
Xiaoping Su ◽  
Erwei Zuo ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Genome Stability ◽  
Mouse Embryos ◽  
Preimplantation Embryos ◽  
End Joining ◽  
Dna Damages ◽  
Developmental Potential ◽  
Damage Repair ◽  
Non Homologous End Joining ◽  
Early Mouse

Abstract Genome stability is critical for the normal development of preimplantation embryos, as DNA damages may result in mutation and even embryo lethality. Anti-silencing factor 1A (ASF1A) is a histone chaperone and enriched in the MII oocytes as a maternal factor, which may be associated with the maintenance of genome stability. Thus, this study was undertaken to explore the role of ASF1A in maintaining the genome stability of early mouse embryos. The ASF1A expressed in the preimplantation embryos and displayed a dynamic pattern throughout the early embryonic development. Inhibition of ASF1A expression decreased embryonic development and increased DNA damages. Overexpression of ASF1A improved the developmental potential and decreased DNA damages. When 293T cells that had been integrated with RGS-NHEJ were co-transfected with plasmids of pcDNA3.1-ASF1A, gRNA-NHEJ, and hCas9, less cells expressed eGFP, indicating that non-homologous end joining was reduced by ASF1A. When 293T cells were co-transfected with plasmids of HR-donor, gRNA-HR, hCas9, and pcDNA3.1-ASF1A, more cells expressed eGFP, indicating that homologous recombination (HR) was enhanced by ASF1A. These results indicate that ASF1A may be associated with the genome stability maintenance of early mouse embryos and this action may be mediated by promoting DNA damage repair through HR pathway.

scholarly journals Gram-Negative Bacterial LPS Induced Poor Uterine Receptivity and Implantation Failure in Mouse: Alterations in IL-1β Expression in the Preimplantation Embryo and Uterine Horns

2005 ◽  
Vol 13 (3) ◽  
pp. 125-133 ◽  
Author(s):  
Kaushik Deb ◽  
Madan Mohan Chaturvedi ◽  
Yogesh Kumar Jaiswal
Keyword(s):  
Cross Sections ◽  
Pregnancy Loss ◽  
Embryo Implantation ◽  
Preimplantation Embryos ◽  
Soluble Form ◽  
Implantation Failure ◽  
Perinatal Complications ◽  
Uterine Receptivity ◽  
Gram Negative ◽  
Blastocyst Implantation

Genito-urinary tract or systemic infections of the gram-negative bacteria in pregnant women, causes abortions, preterm labor, and several other perinatal complications. LPS is the most potent antigenic component of the gram-negative bacterial cell wall and is known to modulate the expression of various proinflammatory cytokines. Here we investigate the role of the soluble form of IL-1 i.e., IL-1β in the ‘minimum dose’ of LPS induced pregnancy loss in mice. Uterine cross-sections on each day of the preimplantation period of pregnancy were examined histopathologically for finding out LPS induced changes in the uterine preparation for embryo implantation. The expression of IL-1β in the various stages of the preimplantation period of pregnancy was studied by RT-PCR in the embryos and the uterine horns of the LPS treated and normal pregnant mice. We found that LPS significantly alters the proliferation of the glandular epithelium, luminal epithelium and stroma during the preimplantation period. We also found large infiltration of macrophages into the uterine horns of the LPS treated animals. The level and pattern of IL-1β expression in the preimplantation embryos and uterine horns were also altered in LPS treated animals. These observations indicate that LPS can alter the uterine preparation for blastocyst implantation, which could be due to the change in the IL-1β expression in the uterine horns. However, a change in the expression pattern of IL-1β in the preimplantation embryos underlines the significance of this molecule in LPS induced pregnancy loss or implantation failure in mouse.

scholarly journals Live imaging YAP signaling in vivo with fusion reporter mice

2021 ◽  
Author(s):  
Bin Gu ◽  
Brian Bradshaw ◽  
Min Zhu ◽  
Yu Sun ◽  
Sevan Hopyan ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Cell Polarity ◽  
Near Infrared ◽  
Kinase Activity ◽  
Live Imaging ◽  
Mouse Line ◽  
Reporter Mouse ◽  
Reporter Mice ◽  
Mammalian Embryonic Development

YAP protein is a critical regulator of mammalian embryonic development. By generating a near-infrared fusion YAP reporter mouse line, we have achieved high-resolution live imaging of YAP localization during mouse embryonic development. We have validated the reporter by demonstrating its predicted responses to blocking Lats kinase activity or blocking cell polarity. The YAP fusion reporter mice and imaging methods will open new opportunities for understanding dynamic YAP signaling in vivo in many different situations.

scholarly journals Perspective: One-Cell and Cleavage-Stage Mouse Embryos Thrive in Hyperosmotic Oviductal Fluid Through Expression of a Glycine Neurotransmitter Transporter and a Glycine-Gated Chloride Channel: Clinical and Transgenerational Implications

2020 ◽  
Vol 11 ◽  
Author(s):  
Lon J. Van Winkle
Keyword(s):  
Chloride Channel ◽  
Well Being ◽  
Mouse Embryos ◽  
Preimplantation Embryos ◽  
Cleavage Stage ◽  
Developmental Abnormalities ◽  
Neurotransmitter Transporter ◽  
Oviductal Fluid

The osmolality of mouse oviductal fluid ranges from about 300 mOsmol/kg in the ampulla 0–3 h post coitus (h p.c.) to more than 350 mOsmol/kg in the isthmus 34–36 h p.c. Thus, it has been surprising to find that development of one-cell and cleavage-stage mouse embryos arrests in vitro in media exceeding 300 mOsmol/kg, and they develop best in unphysiological, hypotonic media. The glycine concentration in oviductal fluid can, however, rescue development in hypertonic media, so physiological conditions in vivo and in vitro likely work together to foster embryo well-being. Glycine acts on one-cell and cleavage-stage mouse embryos through the glycine-gated chloride channel, GLRA4, and uptake via the glycine neurotransmitter transporter, GLYT1. Since these processes lead to further signaling in neurons, the presence and function of such signaling in preimplantation embryos also should be investigated. The more we know about the interactions of physiological processes and conditions in vivo, the better we would be able to reproduce them in vitro. Such improvements in assisted reproductive technology (ART) could improve patient outcomes for IVF and potentially help prevent unwanted developmental abnormalities in early embryos, which might include undesirable epigenetic DNA and histone modifications. These epigenetic modifications may lead to transgenerational adult disorders such as metabolic syndrome and related conditions.

scholarly journals Homeostatic regulation of lipid droplet content in mammalian oocytes and embryos

Reproduction ◽  
2021 ◽  
Vol 162 (6) ◽  
pp. R99-R109
Author(s):  
Megumi Ibayashi ◽  
Ryutaro Aizawa ◽  
Junichiro Mitsui ◽  
Satoshi Tsukamoto
Keyword(s):  
Embryonic Development ◽  
Lipid Droplets ◽  
Neutral Lipids ◽  
Mammalian Species ◽  
Early Embryonic Development ◽  
Preimplantation Embryos ◽  
Physiological Importance ◽  
Bovine Oocytes ◽  
Mammalian Embryonic Development ◽  
Development Proceeds

Lipid droplets (LDs) consist of a core of neutral lipids such as triacylglycerols and cholesteryl esters covered by a phospholipid monolayer. Recent studies have shown that LDs not only store neutral lipids but are also associated with various physiological functions. LDs are found in most eukaryotic cells and vary in size and quantity. It has long been known that mammalian oocytes contain LDs. Porcine and bovine oocytes contain substantial amounts of LDs, which cause their cytoplasm to darken, whereas mouse and human oocytes are translucent due to their low LD content. A sufficient amount of LDs in mammalian oocytes has been thought to be associated with oocyte maturation and early embryonic development, but the necessity of LDs has been questioned because embryonic development proceeds normally even when LDs are removed. However, recent studies have revealed that LDs play a crucial role during implantation and that maintaining an appropriate amount of LDs is important for early embryonic development, even in mammalian species with low amounts of LDs in their oocytes. This suggests that a fine-tuned balance of LD content is essential for successful mammalian embryonic development. In this review, we discuss the physiological importance of LDs in mammalian oocytes and preimplantation embryos based on recent findings on LD biology.

scholarly journals Maternal Ezh1/2 deficiency in oocyte delays H3K27me2/3 restoration and impairs epiblast development responsible for embryonic sub-lethality in mouse

2021 ◽  
Author(s):  
Yinan Zhao ◽  
Dan Zhang ◽  
Mengying Liu ◽  
Yingpu Tian ◽  
Jinhua Lu ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Gene Knockout ◽  
Epigenetic Modifications ◽  
Preimplantation Embryos ◽  
Polycomb Repressive Complex 2 ◽  
H3k27 Methylation ◽  
Early Embryos ◽  
Gene Knockout Mouse ◽  
Core Components

Mammalian embryonic development is a complex process regulated by various epigenetic modifications. Recently, maternal histone H3 methylations were found to be inherited and reprogrammed in early embryos to regulate embryonic development. The enhancer of zest homolog 1 and 2 (Ezh1 and Ezh2) belong to the core components of Polycomb repressive complex 2 (PRC2) and are the histone methyltransferase of histone 3 lysine 27 (H3K27). How maternal Ezh1 and Ezh2 function on H3K27 methylation in in vivo preimplantation embryos and embryonic development are not clear. Here, we deleted Ezh1 or/and Ezh2 in growing oocytes using gene knockout mouse models, and found that H3K27me3 in oocytes was disappeared by loss of Ezh2 alone while H3K27me2 was absent upon deletion of both Ezh1 and Ezh2. The effects of Ezh1/2 were inherited in maternal knockout zygotes and early embryos, in which restoration of H3K27me3 was delayed until late blastocyte by loss of Ezh2 alone and H3K27me2 was reestablished until morulae by deletion of Ezh1 and Ezh2. However, the ablation of both Ezh1 and Ezh2, but not single Ezh1 or Ezh2, led to significantly decreased litter size due to growth retardation during post-implantation. Furthermore, maternal Ezh1/2 deficiency caused compromised H3K27me3 and pluripotent epiblast cells in late blastocyst, followed by defective development of epiblast. These results demonstrate that in oocytes, Ezh2 is indispensable for H3K27me3 while Ezh1 complements Ezh2 in H3K27me2. Also, maternal Ezh1/2-H3K27 methylation is inherited in descendant embryos and has a critical effect on fetus and placenta development. Thus, this work sheds light on maternal epigenetic modifications during embryonic development.

Abstract 345: Dramatic ATP Depletion Without Concomitant Declines in ATP Synthesis Rates Suggests Impaired Energy Metabolism Mechanisms in Adrenergic-Deficient Mouse Embryos

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Jessica N Peoples ◽  
Candice Baker ◽  
Steven Ebert
Keyword(s):  
Steady State ◽  
Energy Metabolism ◽  
Embryonic Development ◽  
Atp Synthesis ◽  
Mouse Embryos ◽  
Atp Depletion ◽  
Metabolic Substrates ◽  
Energy Demands ◽  
Cardiac Energy

High cardiac energy demands increase during embryonic development, requiring oxidative phosphorylation converting ADP to ATP in mitochondria to meet these demands. We have recently shown that adrenergic hormones are required to maintain sufficient cardiac energy metabolism during embryonic development, but the specific mechanism(s) underlying this regulation are not known. Mouse embryos lacking adrenergic hormones, norepinephrine (NE) and epinephrine (EPI), due to targeted loss of the essential dopamine β-hydroxylase ( Dbh ) gene, have remarkably decreased steady-state ATP/ADP ratios. To determine if ATP synthesis was affected, we examined the rate of ATP formation in adrenergic-deficient and control embryonic hearts. Our rate data have shown that despite > 50-fold decrease of steady-state ATP concentrations in Dbh -/- embryos, the rate of ATP synthesis was not significantly different in adrenergic-competent and deficient embryos. This indicates that respiratory complexes in mitochondria are capable of producing ATP in adrenergic-deficient embryos, and suggest that ATP is either consumed at a faster rate than it is produced or its production is limited in vivo due to limited access to metabolic substrates (“starvation”). These findings reveal new mechanistic insights about how adrenergic hormones regulate energy metabolism during embryonic development.

scholarly journals Pak2 reduction induces a failure of early embryonic development in mice

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Juan Zeng ◽  
Nengqing Liu ◽  
Yinghong Yang ◽  
Yi Cheng ◽  
Yuanshuai Li ◽  
...  
Keyword(s):  
Dna Repair ◽  
Embryonic Development ◽  
Cell Apoptosis ◽  
Spindle Assembly ◽  
Dna Lesions ◽  
Mouse Embryos ◽  
Early Embryonic Development ◽  
Preimplantation Embryos ◽  
Early Mouse

Abstract Background The quality of the early embryo is vital to embryonic development and implantation. As a highly conserved serine/threonine kinase, p21-activated kinase 2 (Pak2) participates in diverse biologic processes, especially in cytoskeleton remodeling and cell apoptosis. In mice, Pak2 knock out and endothelial depletion of Pak2 showed embryonic lethality. However, the role of Pak2 in preimplantation embryos remains unelucidated. Methods In the present work, Pak2 was reduced using a specific small interfering RNA in early mouse embryos, validating the unique roles of Pak2 in spindle assembly and DNA repair during mice early embryonic development. We also employed immunoblotting, immunostaining, in vitro fertilization (IVF) and image quantification analyses to test the Pak2 knockdown on the embryonic development progression, spindle assembly, chromosome alignment, oxidative stress, DNA lesions and blastocyst cell apoptosis. Areas in chromatin with γH2AX were detected by immunofluorescence microscopy and serve as a biomarker of DNA damages. Results We found that Pak2 knockdown significantly reduced blastocyst formation of early embryos. In addition, Pak2 reduction led to dramatically increased abnormal spindle assembly and chromosomal aberrations in the embryos. We noted the overproduction of reactive oxygen species (ROS) with Pak2 knockdown in embryos. In response to DNA double strand breaks (DSBs), the histone protein H2AX is specifically phosphorylated at serine139 to generate γH2AX, which is used to quantitative DSBs. In this research, Pak2 knockdown also resulted in the accumulation of phosphorylated γH2AX, indicative of increased embryonic DNA damage. Commensurate with this, a significantly augmented rate of blastocyst cell apoptosis was detected in Pak2-KD embryos compared to their controls. Conclusions Collectively, our data suggest that Pak2 may serve as an important regulator of spindle assembly and DNA repair, and thus participate in the development of early mouse embryos.

scholarly journals Pak2 Depletion Induces a Failure of Early Embryonic Development in Mice

2021 ◽  
Author(s):  
Juan Zeng ◽  
Nengqing Liu ◽  
Yinghong Yang ◽  
Yi Cheng ◽  
Yuanshuai Li ◽  
...  
Keyword(s):  
Dna Repair ◽  
Embryonic Development ◽  
Cell Apoptosis ◽  
Spindle Assembly ◽  
Dna Lesions ◽  
Mouse Embryos ◽  
Early Embryonic Development ◽  
Preimplantation Embryos ◽  
Early Mouse

Abstract Background: The quality of the early embryo is vital to embryonic development and implantation. As a highly conserved serine/threonine kinase, p21-activated kinase 2 (Pak2) participates in diverse biologic processes, especially in cytoskeleton remodeling and cell apoptosis. However, the role of Pak2 in preimplantation embryos remains unelucidated. Methods: In the present work, Pak2 was depleted using a specific small interfering RNA in early mouse embryos, validating the unique roles of Pak2 in spindle assembly and DNA repair during mice early embryonic development. We also employed immunoblotting, immunostaining, in vitro fertilization (IVF) and image quantification analyses to test the Pak2 knockdown on the embryonic development progression, spindle assembly, chromosome alignment, oxidative stress, DNA lesions and blastocyst cell apoptosis.Results: We found that Pak2 deletion significantly reduced blastocyst formation of early embryos. In addition, Pak2 depletion led to dramatically increased abnormal spindle assembly and chromosomal aberrations in the embryos. We noted the overproduction of reactive oxygen species (ROS) with Pak2 knockdown in embryos. Pak2 knockdown also resulted in the accumulation of phosphorylated γH2AX, indicative of increased embryonic DNA damage. Commensurate with this, a significantly augmented rate of blastocyst cell apoptosis was detected in Pak2-KD embryos compared to their controls. Conclusions: Collectively, our data suggest that Pak2 may serve as an important regulator of spindle assembly and DNA repair, and thus participate in the development of early mouse embryos.

Effect of culture in vitro and organ culture on the dry mass of preimplantation mouse embryos

1994 ◽  
Vol 6 (2) ◽  
pp. 229 ◽  
Author(s):  
K Turner ◽  
AW Rogers ◽  
EA Lenton
Keyword(s):  
Organ Culture ◽  
Culture System ◽  
Dry Mass ◽  
Mouse Embryos ◽  
Preimplantation Embryos ◽  
Cell Stage ◽  
Organ Culture System ◽  
Preimplantation Mouse

The dry mass of mouse embryos cultured in vitro in medium alone or in an organ culture system were measured by means of the Vickers M86 scanning microinterferometer. The data were compared with previous data on the dry mass of preimplantation embryos in vivo. The metabolism of embryos cultured in vitro differs from that of fresh embryos. In cultured embryos, dry mass decreases throughout the 2-cell stage whereas the dry mass is increasing at this stage in vivo. Embryos in an organ culture system regain a dry mass profile, similar to that observed in vivo at the late cleavage stage. These results support the view that conditions for embryo metabolism are suboptimal in vitro and that, although the oviduct may confer some advantage on developing embryos in vitro, it is unable fully to support the pattern of metabolism, as assessed by dry mass, observed in vivo.

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