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Journal articles on the topic 'Foetal mouse'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Meek, Jennifer, and Eileen D. Adamson. "Transferrin in foetal and adult mouse tissues: synthesis, storage and secretion." Development 86, no. 1 (April 1, 1985): 205–18. http://dx.doi.org/10.1242/dev.86.1.205.

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Transferrin is an important growth-promoting serum glycoprotein synthesized chiefly in the liver in adults. The transferrin found in the mouse foetus is thought to be wholly a product of the foetus itself and its synthesis starts at least as early as the 7th day of gestation. The major sites of synthesis in mouse foetuses are the visceral yolk sac (VYS) and liver (Adamson, 1982). We now report that other murine foetal tissues synthesize readily detectable amounts, namely lung, spleen, spinal cord and rib cage. Very low levels are also synthesized by the brain, muscle and pancreas. We can detect no synthesis of transferrin in late foetal thymus, heart or skin although mid-gestation foetal skin may make a very small amount. No synthesis of transferrin can be detected in adult brain, lung and spleen, but approximately equal rates of synthesis are detected in adult liver and adult ear pinna. Transferrin is accumulated by foetal and adult tissues in widely varying amounts and these have been measured by enzyme-linked immunosorbent assays of extracts. In addition to VYS and liver, high levels of transferrin are found in foetal skin, lung and rib cage with lower amounts in spinal cord, spleen and muscle tissues. Tissues of the 15th day foetus accumulate the highest concentrations of transferrin. A role for the mediation of transferrin in the stimulation of growth and differentiation by interacting tissues is discussed.

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2

Ceredig, R. "Mouse foetal thymus development." Research in Immunology 141, no. 3 (1990): 286–89. http://dx.doi.org/10.1016/0923-2494(90)90125-i.

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3

Bro-Rasmussen, Frede, and O. Henriksen. "Foetal Erythropoiesis in the Mouse." Scandinavian Journal of Haematology 1, no. 1 (April 24, 2009): 26–37. http://dx.doi.org/10.1111/j.1600-0609.1964.tb00003.x.

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4

Kershaw, T. R., and J. D. Sinden. "Survival of Foetal Neural Tissue from the H-2Kb-tsA58 Transgenic Mouse Grafted to Adult Mouse Brain." Cell Transplantation 2, no. 3 (May 1993): 215–22. http://dx.doi.org/10.1177/096368979300200305.

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Many recent studies have used a temperature sensitive strain of the simian virus 40 large tumor antigen gene (tsA58) to immortalise foetal neural cells by gene insertion in vitro. The H-2Kb-tsA58 transgenic mouse circumvents the need for such genetic manipulation as the tsA58 gene is already within its genome. The results from this study show that foetal neural cells from this mouse do no proliferate and form tumors after grafting to adult brain; rather they survive and differentiate in a manner similar to nontransgenic foetal neural transplants. Therefore, this mouse is a potential source of cells for generating cell lines useful for transplantation studies.

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5

Reiksson, Margareta. "SALICYLATE-INDUCED FOETAL HAEMORRHAGE IN TWO MOUSE STRAINS." Acta Pathologica Microbiologica Scandinavica 76, no. 2 (August 18, 2009): 164–70. http://dx.doi.org/10.1111/j.1699-0463.1969.tb03247.x.

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6

Carroll, Mark, and Margaret M. Bird. "Glycoprotein expression in foetal and adult mouse cerebellum." Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 95, no. 4 (January 1990): 855–60. http://dx.doi.org/10.1016/0305-0491(90)90328-q.

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7

McCloghry, CE, DE Hollis, A. Foldes, AJ Rintoul, P. Baker, JD Vaughan, CA Maxwell, JP Kennedy, and PC Wynn. "The effects of exogenous melatonin and prolactin on wool follicle development in ovine foetal skin grafts." Australian Journal of Agricultural Research 44, no. 5 (1993): 993. http://dx.doi.org/10.1071/ar9930993.

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The fleece of the Merino sheep is composed predominantly of wool fibres grown from secondary wool follicles. This study investigates the effects of melatonin and prolactin on the development of secondarv follicles in grafted ovine foetal skin. Skin from day 85 ovine foetuses was grafted onto nude mice, developed for 40 days and then excised. Mice received either 30 8g prolactin ip mouse-1 day-1 (P), one melatonin implant (Regulin�) sc mouse -1 (M), commencing at grafting or no further treatment (C). Wool follicle density and development were assessed in grafted skin and compared with day 125 control foetal skin. Cuticle structure of graft fibres was also examined and compared with those of day 125 foetuses. Total follicle density and the rate of follicle initiation were reduced in the grafts compared with control foetal skin. Total follicle density did not vary significantly between treatments, but the number of derived secondary follicles was greater in grafts from mice receiving prolactin (group P). Follicles in grafted skin were larger, produced medullated fibres, and were not grouped, in comparison with follicles in the control foetal skin. Epidermal thickness was greater in grafts than in control foetal skin. The cuticle structure of graft fibres from all groups was similar to the control wool fibres. These findings indicate that prolactin, but not melatonin, may be involved in the regulation of derived secondary follicle development.

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8

Airey, Chris J., Phoebe J. Smith, Katie Restall, Stephanie J. Marfy‐Smith, Tom P. Fleming, and Sandrine Willaime‐Morawek. "ISDN2014_0241: Maternal undernutrition affects neurogenesis in the foetal mouse brain." International Journal of Developmental Neuroscience 47, Part_A (December 2015): 72. http://dx.doi.org/10.1016/j.ijdevneu.2015.04.197.

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9

Kovarik, Jiri, Maria Koulmanda, and Thomas E. Mandel. "The role of cytokines during rejection of foetal pig and foetal mouse pancreas grafts in nonobese diabetic mice." Transplant Immunology 5, no. 4 (December 1997): 307–14. http://dx.doi.org/10.1016/s0966-3274(97)80014-7.

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10

SAIDA, Kaname, Naoko KOMETANI, Tsuyoshi UCHIDE, and Youji MITSUI. "Sequence analysis and expression of the mouse full-length vasoactive intestinal contractor/endothelin-2 gene (EDN2): comparison with the endothelin-1 gene (EDN1)." Clinical Science 103, s2002 (September 1, 2002): 84S—89S. http://dx.doi.org/10.1042/cs103s084s.

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Vasoactive intestinal contractor (VIC)/endothelin-2 (ET2) is a vasoactive peptide hormone comprising 21 amino acids. The complete nucleotide sequence of the full-length gene encoding preproVIC (PPVIC) was determined. The PPVIC gene contains five exons that span 6kb and shows a duplication on exons 2 and 3, coding for the VIC and VIC-like peptides respectively. Similarities between the genomic organization of the PPVIC/preproET2 and preproendothelin-1 genes suggest that the two are distantly related. PPVIC gene expression was observed in foetal and adult mouse intestine. The expression level in adults was approx. 10-fold higher than in the foetus, suggesting an involvement of VIC in intestinal development.

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11

Pribenszky, Csaba, Sándor Cseh, Zsolt Abonyi-Tóth, and László Solti. "Survival of rapidly frozen hatched mouse blastocysts." Zygote 11, no. 4 (November 2003): 361–66. http://dx.doi.org/10.1017/s0967199403002417.

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The objective of the present study was to examine the effect of rapid freezing on the in vitro and in vivo survival of zona-pellucida-free hatched mouse blastocysts. Hatched blastocysts were rapidly frozen in a freezing medium containing either ethylene glycol (EG) or glycerol (G) in 1.5 M or 3 M concentration. Prior to freezing, embryos were equilibrated in the freezing medium for 2 min, 10 min, 20 min or 30 min at room temperature. To freeze them, embryos were held in liquid nitrogen vapour [≈1 cm above the surface of the liquid nitrogen (LN2)] for 2 minutes and then immersed into LN2. After thawing, embryos were transferred either to rehydration medium (DPBS + 10% foetal calf serum + 0.5 M sucrose) for 10 minutes or rehydrated directly in DPBS supplemented with foetal calf serum. In vitro survival of embryos frozen with EG was higher than those frozen with G. The highest survival was obtained with 3 M EG and 2 min or 10 min equilibration prior to freezing, combined with direct rehydration after thawing. Frozen blastocysts developed into normal foetuses as well as unfrozen control ones did, with averages of 30% (control), 26% (EG) and 15% (G). The results show that hatching and hatched mouse blastocysts can be cryopreserved by a simple rapid freezing protocol in EG without significant loss of viability. Our data indicate that the mechanical protection of the zona pellucida is not needed during freezing in these stages.

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12

Coppen, Steven R., Riyaz A. Kaba, Robert G. Gourdie, Jeremy N. Skepper, Suzy Elneil, and Nicholas J. Severs. "Connexin expression in the developing mouse heart and human foetal heart." Journal of Molecular and Cellular Cardiology 33, no. 6 (June 2001): A23. http://dx.doi.org/10.1016/s0022-2828(01)90091-4.

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13

Tease, C., and G. Fisher. "Further examination of the production-line hypothesis in mouse foetal oocytes." Chromosoma 97, no. 4 (January 1989): 315–20. http://dx.doi.org/10.1007/bf00371972.

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14

Tease, C., and G. Fisher. "Further examination of the production-line hypothesis in mouse foetal oocytes." Chromosoma 93, no. 5 (April 1986): 447–52. http://dx.doi.org/10.1007/bf00285827.

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15

Piliszek, Anna, Jacek A. Modliński, Kazimiera Pyśniak, and Jolanta Karasiewicz. "Foetal fibroblasts introduced to cleaving mouse embryos contribute to full-term development." Reproduction 133, no. 1 (January 2007): 207–18. http://dx.doi.org/10.1530/rep-06-0013.

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Foetal fibroblasts (FFs) labelled with vital fluorescent dye were microsurgically introduced into eight-cell mouse embryos, three cells to each embryo. FFs were first identified in the inner cell mass (ICM) in about one-third of embryos, whereas in three quarters of embryos FFs were located among trophoblast cells. Some elimination of FFs from trophoblast occurred later on. Eventually, in blastocysts’ outgrowths, an equally high contribution from FFs progeny (60%) was found in both ICM and trophoblast. Three days after manipulation, FFs resumed proliferation in vitro. More than three FFs were found in 46.2% of embryos on day 4. On the 7th day in vitro in 70% of embryos more than 12 FFs were found, proving at least three cell divisions. To study postimplantation development, the embryos with FFs were transferred to pseudopregnant recipients a day after manipulation. After implantation, FFs were identified by electrophoresis for isozymes of glucose phosphate isomerase (GPI). A single 11-day embryo delayed to day 8 proved chimeric by expressing both donor isozyme GPI-1B and recipient GPI-1A. Similar chimerism was found in the extraembryonic lineage of 11% of embryos by day 12. Starting from day 11 onwards, in 32% of normal embryos and in 57% of foetal membranes, hybrid GPI-1AB isozyme, as well as recipient isozyme, was present. Hybrid GPI-1AB can only be produced in hybrid cells derived by cell fusion, therefore, we suggest that during postimplantation development, FFs are rescued by fusion with recipient cells. In the mice born, hybrid isozyme was found in several tissues, including brain, lung, gut and kidney. We conclude that somatic cells (FFs) can proliferate in earlyembryonic environment until early postimplantation stages. Foetuses and the mice born are chimeras between recipient cells and hybrid cells with contributions from the donor FFs. Transdifferentiation as opposed to reprogramming by cell fusion can be considered as underlying cellular processes in these chimeras.

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16

DEVI, P. UMA. "Effect of gamma radiation on the foetal haemopoietic system in the mouse." International Journal of Radiation Biology 74, no. 5 (January 1998): 639–46. http://dx.doi.org/10.1080/095530098141221.

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17

Dimberg, Y. "Effects of single dose and fractionated irradiation on foetal mouse brain aggregates." Toxicology in Vitro 11, no. 3 (June 1997): 193–200. http://dx.doi.org/10.1016/s0887-2333(97)00010-6.

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18

Forand, A., S. Messiaen, R. Habert, and J. Bernardino-Sgherri. "Exposure of the mouse perinatal testis to radiation leads to hypospermia at sexual maturity." REPRODUCTION 137, no. 3 (March 2009): 487–95. http://dx.doi.org/10.1530/rep-08-0358.

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The first round of mouse spermatogenesis begins from 3 to 4 days after birth through differentiation of gonocytes into spermatogonial-stem cells and type A spermatogonia. Consequently, this step of differentiation may determine generation of the original population of stem cells and the fertility potential of the adult mouse. We aimed to determine the effect of perinatal exposure to ionizing radiation on the testis at the end of the first wave of spermatogenesis and at sexual maturity. Our results show that, radiation sensitivity of the testis substantially decreases from late foetal life to the end of the first week after birth. In addition, partial or full recovery from radiation induced testicular weight loss occurred between the first round of spermatogenesis and sexual maturity, and this was associated with the stimulation of spermatogonial proliferation. Exposure of mice at 17.5 days after conception or at 1 day after birth to γ-rays decreased the sperm counts at sexual maturity, while exposure of 8 day-old mice had no effect. This suggests that irradiation of late foetal or early neonatal testes has a direct impact on the generation of the neonatal spermatogonial-stem cell pool.

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19

Gurner, Kathryn H., Thi T. Truong, Alexandra J. Harvey, and David K. Gardner. "A combination of growth factors and cytokines alter preimplantation mouse embryo development, foetal development and gene expression profiles." Molecular Human Reproduction 26, no. 12 (November 5, 2020): 953–70. http://dx.doi.org/10.1093/molehr/gaaa072.

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Abstract Within the maternal tract, the preimplantation embryo is exposed to an array of growth factors (GFs) and cytokines, most of which are absent from culture media used in clinical IVF. Whilst the addition of individual GFs and cytokines to embryo culture media can improve preimplantation mouse embryo development, there is a lack of evidence on the combined synergistic effects of GFs and cytokines on embryo development and further foetal growth. Therefore, in this study, the effect of a combined group of GFs and cytokines on mouse preimplantation embryo development and subsequent foetal development and gene expression profiles was investigated. Supplementation of embryo culture media with an optimised combination of GFs and cytokines (0.05 ng/ml vascular endothelial GF, 1 ng/ml platelet-derived GF, 0.13 ng/ml insulin-like GF 1, 0.026 ng/ml insulin-like GF 2 and 1 ng/ml granulocyte colony-stimulating factor) had no effect on embryo morphokinetics but significantly increased trophectoderm cell number (P = 0.0002) and total cell number (P = 0.024). Treatment with this combination of GFs and cytokines also significantly increased blastocyst outgrowth area (P < 0.05) and, following embryo transfer, increased foetal weight (P = 0.027), crown-rump length (P = 0.017) and overall morphological development (P = 0.027). RNA-seq analysis of in vitro derived foetuses identified concurrent alterations to the transcriptional profiles of liver and placental tissues compared with those developed in vivo, with greater changes observed in the GF and cytokine treated group. Together these data highlight the importance of balancing the actions of such factors for the regulation of normal development and emphasise the need for further studies investigating this prior to clinical implementation.

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20

Bartlett, Richard S., and Hans van Wijk. "Feasibility of mouse continuous intravenous infusion for fertility and embryo-foetal development studies." Reproductive Toxicology 34, no. 2 (September 2012): 157. http://dx.doi.org/10.1016/j.reprotox.2012.05.045.

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21

SINJARI, T., and P. O. DARNERUD. "Hydroxylated polychlorinated biphenyls : placental transfer and effects on thyroxine in the foetal mouse." Xenobiotica 28, no. 1 (January 1998): 21–30. http://dx.doi.org/10.1080/004982598239722.

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22

Ito, Keiichi, Ayaka Yanagida, Ken Okada, Yuji Yamazaki, Hiromitsu Nakauchi, and Akihide Kamiya. "Mesenchymal progenitor cells in mouse foetal liver regulate differentiation and proliferation of hepatoblasts." Liver International 34, no. 9 (December 4, 2013): 1378–90. http://dx.doi.org/10.1111/liv.12387.

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23

Stolp, H. B., C. Turnquist, K. M. Dziegielewska, N. R. Saunders, D. C. Anthony, and Z. Molnar. "Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse." Brain 134, no. 11 (September 29, 2011): 3236–48. http://dx.doi.org/10.1093/brain/awr237.

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24

MANOLOV, G., I. URUMOV, R. ARGIROVA, and P. PETKOVA. "Cytogenetic study of foetal colon mouse tumour-AKATOL-1-71-cultivated in vitro." Hereditas 90, no. 2 (February 12, 2009): 227–36. http://dx.doi.org/10.1111/j.1601-5223.1979.tb01310.x.

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25

Labied, S., C. Munaut, S. Blacher, N. Coqué, O. Sandra, A. Noël, P. Carmeliet, J.-M. Foidart, and F. Frankenne. "ABSTRACTS: 2 Mouse PAI-1 promotes placentation by increasing foetal and maternal angiogenesis." American Journal of Reproductive Immunology 60, no. 1 (June 28, 2008): 85–86. http://dx.doi.org/10.1111/j.1600-0897.2008.00626_2.x.

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26

Fullston, T., M. Mitchell, S. Wakefield, A. Filby, and M. Lane. "130. MICROARRAY ANALYSIS OF FOETAL MOUSE BRAIN FOLLOWING INDUCTION OF MITOCHONDRIAL DYSFUNCTION DURING PRE-IMPLANTATION EMBRYO DEVELOPMENT." Reproduction, Fertility and Development 21, no. 9 (2009): 49. http://dx.doi.org/10.1071/srb09abs130.

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Environmental stress can disrupt mitochondrial function in the pre-implantation embryo, subsequently hindering embryo viability. Brain tissue is also sensitive to developmental perturbations, and we have previously discovered genes involved in neurological function and epigenetic modification are differentially expressed in blastocysts following mitochondrial dysfunction by amino-oxyacetate (AOA). In this study CBAxC57Bl6 2 cell stage mouse embryos were cultured in 5μM-AOA without pyruvate for 72h to induce mitochondrial dysfunction. Blastocyst stage embryos were then transferred to pseudopregnant recipients and the expression profile of day 18 foetal brains was interrogated using microarray. mRNA from mouse whole brain (4 per treatment) was extracted and analysed using an Affymetrix gene array. Ingenuity Pathway Analysis software identified persistent alterations in gene expression pathways in foetal brain after AOA treatment during embryo culture, that were subsequently confirmed by qPCR. Expression was significantly increased by both array and qPCR (>1.5 fold, p<0.05) for; 1) Eomes (1.9, 2.9 fold respectively), a T-box transcription factor involved in differentiation, cell death and development, 2) Nr4a3 (1.8, 2.2 fold respectively), a steroid hormone receptor and putative transcriptional activator and 3) Nola3 (1.7, 1.9 fold respectively), a small nucleolar ribonucleoprotein involved in rRNA processing. Neurological disease, behavioural disorders, carbohydrate metabolism, cellular growth and proliferation, cell death, DNA replication, recombination and repair pathways also showed altered gene expression (>1.25 fold). qPCR was performed on 28 genes exhibiting the greatest change in expression. 24/28 genes confirmed the array data, and of the 4 genes that did not; two had expression not detected by qPCR (Snhg1, Speer6-ps1), and two contradicted array results (Atp1b3 p=0.05, Stk38l p=0.06). This study links mitochondrial dysfunction during early embryo development and persistent molecular changes in the developing foetal brain. This indicates that insults incurred during early embryo development can cause permanent changes that we predict results from aberrant epigenetic modification.

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27

Wang, Fuchuan, Guangming Cao, Wei Yi, Li Li, and Xiuzhen Cao. "Effect of Metformin on a Preeclampsia-Like Mouse Model Induced by High-Fat Diet." BioMed Research International 2019 (December 7, 2019): 1–8. http://dx.doi.org/10.1155/2019/6547019.

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Background. Metformin has been reported to decrease insulin resistance and is associated with a lower risk of pregnancy-induced hypertension and preeclampsia. It is widely accepted that the placenta plays a crucial role in the development of preeclampsia. Our aim is to explore the effect of metformin on preeclampsia. Study Design. We examined control diet-fed (isocaloric diet) pregnant mice (CTRL group), pregnant mice fed a high-fat diet (HF group), and high-fat-diet-fed pregnant mice treated with metformin (HF-M group). The HF mice were fed a high-fat diet six weeks before pregnancy to establish a preeclampsia-like model; then, the group was randomly divided into a HF group and a HF-M group after pregnancy. Blood pressure, urine protein, pregnancy outcomes, protein expression, and histopathological changes in the placentas of all groups were examined and statistically analysed. Results. We observed that metformin significantly improved high blood pressure, proteinuria, and foetal and placental weights in the HF-M group compared with the HF group. Metformin significantly improved placental labyrinth and foetal vascular development in preeclampsia. In addition, metformin effectively increased matrix metalloproteinase-2 (MMP-2) and vascular endothelial growth factor (VEGF) levels in the placenta. Conclusions. Our results suggest that metformin can improve preeclamptic symptoms and pregnancy outcomes.

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28

Simon, François, Françoise Denoyelle, and Mathieu Beraneck. "Interpreting pendred syndrome as a foetal hydrops: Clinical and animal model evidence." Journal of Vestibular Research 31, no. 4 (July 28, 2021): 315–21. http://dx.doi.org/10.3233/ves-200789.

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BACKGROUND: Menière disease (MD) and SLC26A4 related deafness (Pendred syndrome (PS) or DFNB4) are two different inner ear disorders which present with fluctuating and progressive hearing loss, which could be a direct consequence of endolymphatic hydrops. OBJECTIVE: To present similarities between both pathologies and explore how the concept of hydrops may be applied to PS/DFNB4. METHODS: Review of the literature on MD, PS/DFNB4 and mouse model of PS/DFNB4. RESULTS: MD and PS/DFNB4 share a number of similarities such as fluctuating and progressive hearing loss, acute episodes with vertigo and tinnitus, MRI and histological evidence of endolymphatic hydrops (although with different underlying mechanisms). MD is usually diagnosed during the fourth decade of life whereas PS/DFNB4 is congenital. The PS/DFNB4 mouse models have shown that biallelic slc26a4 mutations lead to Na+ and water retention in the endolymph during the perinatal period, which in turn induces degeneration of the stria vascularis and hearing loss. Crossing clinical/imagery characteristics and animal models, evidence seems to support the hypothesis of PS being a foetal hydrops. CONCLUSIONS: When understanding PS/DFNB4 as a developmental hydrops, treatments used in MD could be repositioned to PS.

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29

Mackay, Sarah, and Robert A. Smith. "The differentiation of mouse gonads in vitro: a light and electron microscopical study." Development 97, no. 1 (September 1, 1986): 189–99. http://dx.doi.org/10.1242/dev.97.1.189.

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Indifferent urogenital complexes were excised from mouse foetuses assessed by developmental criteria as day 10·5 or 11. After 4 or 6–7 days in culture, complexes were fixed and examined by light and electron microscopy. The effect of culturing sexed complexes in mixed sex groups was investigated. The effect of the presence or absence of foetal calf serum in the culture medium was considered. No evidence of inhibition of one sex by the other was found. Ovaries developed further in cultures than testes.

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30

Ikeda, Keiko, Adriana A. Tienda, Fiona E. Harrison, and Kiyoshi Kawakami. "Decreased content of ascorbic acid (vitamin C) in the brain of knockout mouse models of Na+,K+-ATPase-related neurologic disorders." PLOS ONE 16, no. 2 (February 5, 2021): e0246678. http://dx.doi.org/10.1371/journal.pone.0246678.

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Na+,K+-ATPase is a crucial protein responsible for maintaining the electrochemical gradients across the cell membrane. The Na+,K+-ATPase is comprised of catalytic α, β, and γ subunits. In adult brains, the α3 subunit, encoded by ATP1A3, is predominantly expressed in neurons, whereas the α2 subunit, encoded by ATP1A2, is expressed in glial cells. In foetal brains, the α2 is expressed in neurons as well. Mutations in α subunits cause a variety of neurologic disorders. Notably, the onset of symptoms in ATP1A2- and ATP1A3-related neurologic disorders is usually triggered by physiological or psychological stressors. To gain insight into the distinct roles of the α2 and α3 subunits in the developing foetal brain, whose developmental dysfunction may be a predisposing factor of neurologic disorders, we compared the phenotypes of mouse foetuses with double homozygous knockout of Atp1a2 and Atp1a3 (α2α3-dKO) to those with single knockout. The brain haemorrhage phenotype of α2α3-dKO was similar to that of homozygous knockout of the gene encoding ascorbic acid (ASC or vitamin C) transporter, SVCT2. The α2α3-dKO brain showed significantly decreased level of ASC compared with the wild-type (WT) and single knockout. We found that the ASC content in the basal ganglia and cerebellum was significantly lower in the adult Atp1a3 heterozygous knockout mouse (α3-HT) than in the WT. Interestingly, we observed a significant decrease in the ASC level in the basal ganglia and cerebellum of α3-HT in the peripartum period, during which mice are under physiological stress. These observations indicate that the α2 and α3 subunits independently contribute to the ASC level in the foetal brain and that the α3 subunit contributes to ASC transport in the adult basal ganglia and cerebellum. We propose that decreases in ASC levels may affect neural network development and are linked to the pathophysiology of ATP1A2- and ATP1A3-related neurologic disorders.

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31

Hopkinson-Woolley, J., D. Hughes, S. Gordon, and P. Martin. "Macrophage recruitment during limb development and wound healing in the embryonic and foetal mouse." Journal of Cell Science 107, no. 5 (May 1, 1994): 1159–67. http://dx.doi.org/10.1242/jcs.107.5.1159.

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Macrophages play a pivotal role in the adult inflammatory response to wounding. They are directly responsible for cellular debridement and, by providing a source of growth factors and cytokines, they recruit other inflammatory and fibroblastic cells and influence cell proliferation and tissue remodelling. In this paper we investigate the role of macrophages in clearing areas of programmed cell death in the developing embryo and also their role in embryonic and foetal wound healing. Immunocytochemistry using the monocyte/macrophage-specific monoclonal antibody, F4/80, reveals a close association between areas of programmed cell death in the remodelling interdigital regions of the mouse footplate and of F4/80-positive cells, suggesting that monocyte-derived macrophages, and not locally recruited fibroblastic cells, as previously believed, are responsible for phagocytosing and clearing areas of interdigital apoptosis. Our studies of wound healing reveal that macrophages are not recruited to, and therefore cannot be playing an active role in the healing of, excisional wounds made in the mouse embryo at any stage up until E14.5. Beyond this transition stage we see a significant recruitment of macrophages within 12 hours of wounding. We find that macrophages can be attracted to wounds in earlier embryos if the wound results in significant cell death such as after burning.

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32

Pavlos, NJ, J. Xu, JM Papadimitriou, and MH Zheng. "Molecular cloning of the mouse homologue of Rab3c." Journal of Molecular Endocrinology 27, no. 1 (August 1, 2001): 117–22. http://dx.doi.org/10.1677/jme.0.0270117.

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Small GTP-binding proteins of the Rab subfamily are key regulators of intracellular vesicle transport. Here we report the isolation of a cDNA clone encoding the complete Rab3c isoform from mouse embryo using a degenerative PCR-based approach. Multiple sequence alignment revealed that the predicted amino acid sequence was identical to the previously identified rat Rab3c isoform and 98% identical to the published bovine Rab3c GTPase from brain. Furthermore by in situ hybridisation, Rab3c mRNA was detectable within various regions of the brain, cartilage and highly enriched within intestinal villi of foetal tissues. Chondrocytes in the hypertrophic zone, but not reserve or proliferative zones, expressed high levels of Rab3c. This pattern of expression corresponds with the genesis of matrix vesicles during endochondral ossification.In all, our results suggest that in addition to its functional role during regulated secretion in brain, Rab3c may play a part in matrix vesicle trafficking during skeletal development.

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33

Lu, Dan, Jizheng Wang, Jing Li, Feifei Guan, Xu Zhang, Wei Dong, Ning Liu, Shan Gao, and Lianfeng Zhang. "Meox1 accelerates myocardial hypertrophic decompensation through Gata4." Cardiovascular Research 114, no. 2 (November 16, 2017): 300–311. http://dx.doi.org/10.1093/cvr/cvx222.

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AbstractAimsPathological hypertrophy is the result of gene network regulation, which ultimately leads to adverse cardiac remodelling and heart failure (HF) and is accompanied by the reactivation of a ‘foetal gene programme’. The Mesenchyme homeobox 1 (Meox1) gene is one of the foetal programme genes. Meox1 may play a role in embryonic development, but its regulation of pathological hypertrophy is not known. Therefore, this study investigated the effect of Meox1 on pathological hypertrophy, including familial and pressure overload-induced hypertrophy, and its potential mechanism of action.Methods and resultsMeox1 expression was markedly down-regulated in the wild-type adult mouse heart with age, and expression was up-regulated in heart tissues from familial dilated cardiomyopathy (FDCM) mice of the cTnTR141W strain, familial hypertrophic cardiomyopathy (FHCM) mice of the cTnTR92Q strain, pressure overload-induced HF mice, and hypertrophic cardiomyopathy (HCM) patients. Echocardiography, histopathology, and hypertrophic molecular markers consistently demonstrated that Meox1 overexpression exacerbated the phenotypes in FHCM and in mice with thoracic aorta constriction (TAC), and that Meox1 knockdown improved the pathological changes. Gata4 was identified as a potential downstream target of Meox1 using digital gene expression (DGE) profiling, real-time PCR, and bioinformatics analysis. Promoter activity data and chromatin immunoprecipitation (ChIP) and Gata4 knockdown analyses indicated that Meox1 acted via activation of Gata4 transcription.ConclusionMeox1 accelerated decompensation via the downstream target Gata4, at least in part directly. Meox1 and other foetal programme genes form a highly interconnected network, which offers multiple therapeutic entry points to dampen the aberrant expression of foetal genes and pathological hypertrophy.

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Cantacorps, Lídia, Silvia Alfonso-Loeches, Consuelo Guerri, and Olga Valverde. "Long-term epigenetic changes in offspring mice exposed to alcohol during gestation and lactation." Journal of Psychopharmacology 33, no. 12 (June 18, 2019): 1562–72. http://dx.doi.org/10.1177/0269881119856001.

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Background: Alcohol exposure impairs brain development and leads to a range of behavioural and cognitive dysfunctions, termed as foetal alcohol spectrum disorders. Although different mechanisms have been proposed to participate in foetal alcohol spectrum disorders, the molecular insights of such effects are still uncertain. Using a mouse model of foetal alcohol spectrum disorder, we have previously shown that maternal binge-like alcohol drinking causes persistent effects on motor, cognitive and emotional-related behaviours associated with neuroimmune dysfunctions. Aims: In this study, we sought to evaluate whether the long-term behavioural alterations found in offspring with early exposure to alcohol are associated with epigenetic changes in the hippocampus and prefrontal cortex. Methods: Pregnant C57BL/6 female mice underwent a model procedure for binge alcohol drinking throughout both the gestation and lactation periods. Subsequently, adult offspring were assessed for their cognitive function in a reversal learning task and brain areas were extracted for epigenetic analyses. Results: The results demonstrated that early binge alcohol exposure induces long-term behavioural effects along with alterations in histone acetylation (histone H4 lysine 5 and histone H4 lysine 12) in the hippocampus and prefrontal cortex. The epigenetic effects were linked with an imbalance in histone acetyltransferase activity that was found to be increased in the prefrontal cortex of mice exposed to alcohol. Conclusions: In conclusion, our results reveal that maternal binge-like alcohol consumption induces persistent epigenetic modifications, effects that might be associated with the long-term cognitive and behavioural impairments observed in foetal alcohol spectrum disorder models.

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Thum, Caroline, Kikuji Itoh, Wayne Young, Adrian Cookson, Warren McNabb, and Nicole Roy. "Effects of Prenatal Consumption of Caprine Milk Oligosaccharides on Mice Mono-associated with Bifidobacterium Bifidum (AGR2166)." Open Microbiology Journal 11, no. 1 (June 30, 2017): 105–11. http://dx.doi.org/10.2174/1874285801711010105.

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Background:Prenatal consumption of oligosaccharides are associated with changes in the maternal gastrointestinal tract (GIT) microbiota with health consequences for the offspring. It has previously been demonstrated that caprine milk oligosaccharides (CMO) stimulate the growth and fermentation rate ofBifidobacterium bifidumAGR2166.Objective:The objective of this study was to examine the effects ofB. bifidumAGR2166 and prenatal consumption of CMO, alone or in combination, on the dam’s large intestine, foetal development and ability ofB. bifidumto translocate from the gastrointestinal lumen to organs and foetal membranes.Method:Germ-free BALB/c mice, inoculated withB. bifidumAGR2166 or anaerobic phosphate buffer, were fed either diet supplemented with CMO or with galacto-oligosaccharide. Pregnant mice were euthanised 1 to 3 days before the expected delivery date and samples collected for analysis.Results:Dietary CMO, regardless of bifidobacterial inoculation was shown to increase GIT weight and to reduce foetal weight compared to galacto-oligosaccharide-fed dams.B. bifidumAGR2166 DNA was detected in the mesenteric lymph nodes, liver, plasma and placenta of the dam by amplification of the bifidobacterial 16S rRNA gene.Conclusion:B. bifidumAGR2166 DNA was detected in maternal organs, however there is no indication that live bifidobacteria was able to translocate during pregnancy. Further studies using conventionally-raised mouse models will develop a deeper understanding of the interactions between dietary CMOF, the host, and bacteria.

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Rossant, J., and B. A. Croy. "Genetic identification of tissue of origin of cellular populations within the mouse placenta." Development 86, no. 1 (April 1, 1985): 177–89. http://dx.doi.org/10.1242/dev.86.1.177.

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The mouse haemochorial placenta is a complex mixture of maternal cells and foetal trophectoderm and inner cell mass (ICM)-derived cells. The majority of the placental tissue is assumed to be trophoblast in origin but the exact extent and localization of the ICM and maternal contribution has not previously been determined. Using embryo transfer and reconstituted blastocyst techniques, combined with isozymal and in situ genetic markers, we have established that about 70% of the 13 to 15-day placenta is trophectoderm-derived, 30% is maternal in origin, and 4% develops from the ICM. Nearly all of the maternal contribution was confined to the spongiotrophoblast region and all of the ICM contribution was confined to the labyrinthine trophoblast region, where it formed the foetal blood capillaries and the endodermal sinuses. Using the same genetic markers, we showed that cell suspension techniques commonly used to produce ‘trophoblast’ cell preparations from placenta do not enrich for trophoblast, and, indeed, that collagenase, the preferred dissociation technique for cell viability, produced cell suspensions in which ICM and maternal cells were preferentially dissociated. No method for producing pure trophoblast populations has yet been found. Some unusually high ICM contributions to the placenta were found in reconstituted blastocyst experiments using ICMs isolated from early 3·5-day blastocysts, suggesting that these ICMs may have contributed to the trophectoderm layer of the blastocyst. These and other experiments suggest that the inner cell mass lineage may not be closed until some time after formation of the blastocyst.

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West, John D., and Jean H. Flockhart. "Genotypically unbalanced diploid ↔ diploid foetal mouse chimaeras: possible relevance to human confined mosaicism." Genetical Research 63, no. 2 (April 1994): 87–99. http://dx.doi.org/10.1017/s0016672300032195.

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SummaryTwo series of mouse chimaeras were produced by aggregating pairs of eight-cell embryos that differed at the Gpi-1s locus, encoding glucose phosphate isomerase (GPI-1); the paired embryos were respectively homozygous Gpi-1sa/Gpi-1sa and Gpi-1sb/Gpi-1sb. Chimaeric blastocysts were transferred to pseudopregnant females, that were homozygous Gpi-1se/Gpi-1se and produced only GPI-1 C enzyme. Quantitative electrophoresis of GPI-1 was used to estimate the contribution of each embryo (GPI-1 A and GPI-1B enzyme activity) to the foetus, placenta and other extraembryonic tissues of 12½ day chimaericconceptuses. For both series of chimaeras, the distributions of %GPI-1A in different tissues were classified as (1) balanced and typical, (2) balanced but atypical or (3) unbalanced. One series of chimaeras was clearly unbalanced, so that the cells derived from the (C57BL × CBA/Ca)F2 embryo (Gpi-1sb/Gpi-1sb) predominated over those derived from the BALB/c inbred strain (Gpi-1sa/Gpi-1sa) in most foetuses. Two significant observations were made concerning this unbalanced series. Firstly, the mean composition of the placenta and other extraembryonic tissues was similar to that in the foetus i.e. also unbalanced with (C57BL × CBA/Ca)F2 (abbreviated to BF2) cells predominating. Secondly, despite this generalizeddeficiency of BALB/c cells, there were differences in the frequency of non-chimaeric tissues between different developmental lineages. In 20/34 chimaeric conceptuses in the unbalanced series only BF2 cells were detected in the foetus, whereas both BF2 and BALB/c cells were present in at least one of the extraembryonic tissues. This group of chimaeras, therefore, shows some similarities to human confined mosaicism. Although chimaerism occurred more often in the primitive endoderm (hypoblast) lineage (yolk sac endoderm and parietal endoderm) than in the placenta, this may also be the case in human mosaics. The mosaic status of the human yolk sac endoderm is usually unknown so it is possible that mosaicism often occurs in the yolk sac endoderm as well as the trophectoderm in human ‘confined placental mosaicism’. The uniformly unbalanced phenotype seen in the mouse chimaeras may be a result of generalized cell selection against BALB/c cells in all tissues. As an alternative explanation, we propose that most of the BALB/c cells in the blastocyst are allocated to the mural trophectoderm, which has a limited mitotic potential and so contributes little to the mid-gestation conceptus. Further work is required to test these possibilities.

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Buchet, Delphine, Corina Garcia, Cyrille Deboux, Brahim Nait-Oumesmar, and Anne Baron-Van Evercooren. "Human neural progenitors from different foetal forebrain regions remyelinate the adult mouse spinal cord." Brain 134, no. 4 (March 31, 2011): 1168–83. http://dx.doi.org/10.1093/brain/awr030.

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Hossain, P. Uma Devi, M. "Induction of solid tumours in the Swiss albino mouse by low-dose foetal irradiation." International Journal of Radiation Biology 76, no. 1 (January 2000): 95–99. http://dx.doi.org/10.1080/095530000139050.

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Kimura, Naoki, Makiko Takizawa, Keisuke Okita, Osamu Natori, Katsuhide Igarashi, Masaya Ueno, Kin-ichi Nakashima, Ikuo Nobuhisa, and Tetsuya Taga. "Identification of a novel transcription factor, ELYS, expressed predominantly in mouse foetal haematopoietic tissues." Genes to Cells 7, no. 4 (April 2002): 435–46. http://dx.doi.org/10.1046/j.1365-2443.2002.00529.x.

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41

MANOUSSAKA, MARIA, ANDREW GEORGIOU, BETH ROSSITER, SUNIL SHRESTHA, JENNIFER A. TOOMEY, P. V. SIVAKUMAR, MICHAEL BENNETT, VINAY KUMAR, and COLIN G. BROOKS. "NK cell lines of different maturational status can be obtained from mouse foetal liver." Biochemical Society Transactions 25, no. 2 (May 1, 1997): 174S. http://dx.doi.org/10.1042/bst025174s.

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42

Stone, Christopher A. "Unravelling the secrets of foetal wound healing: an insight into fracture repair in the mouse foetus and perspectives for clinical application." British Journal of Plastic Surgery 53, no. 4 (2000): 337–41. http://dx.doi.org/10.1054/bjps.1999.3269.

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43

Beyzavi, K., S. Hampton, P. Kwasowski, S. Fickling, V. Marks, and R. Clift. "Comparison of Horseradish Peroxidase and Alkaline Phosphatase-Labelled Antibodies in Enzyme Immunoassays." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 24, no. 2 (March 1987): 145–52. http://dx.doi.org/10.1177/000456328702400204.

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The periodate method was found to be most effective for preparing horseradish peroxidase-sheep anti-human and horseradish peroxidase-donkey anti-mouse immunoglobulin (IgG) conjugates. The conjugates were improved by carrying out the oxidation of the enzyme at low pH. Anti-human and anti-mouse IgG-peroxidase conjugates (0·5 mg/mL IgG and 0.7 mg/mL 19G, respectively) were used at 1:15 000 and 1:8000 dilutions, respectively, in a sandwich ELISA to detect human and mouse IgG in buffer or in a growth medium containing 20% foetal calf serum. Using the peroxidase conjugates, it was possible to detect human and mouse IgG at concentrations as low as I ng/mL. The glutaraldehyde method was found to be much more effective than the periodate method for conjugating alkaline phosphatase to the antibodies. The optimum dilutions for anti/human and anti-mouse IgG-alkaline phosphatase conjugates (0.18 mg/mL IgG and 0.3 mg/mL IgG, respectively) in ELISA were 1:500 and 1:1000, respectively. The detection limit with alkaline phosphatase conjugates was 7 ng/ml for human IgG and 4 ng/ml for mouse IgG.

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44

Cantacorps, Lídia, Sandra Montagud-Romero, and Olga Valverde. "Curcumin treatment attenuates alcohol-induced alterations in a mouse model of foetal alcohol spectrum disorders." Progress in Neuro-Psychopharmacology and Biological Psychiatry 100 (June 2020): 109899. http://dx.doi.org/10.1016/j.pnpbp.2020.109899.

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45

Suneetha, N., and R. P. Surendra Kumar. "Enzymatic studies in foetal brain and liver of mouse following in utero exposure to ultrasound." Ultrasonics 29, no. 3 (May 1991): 257–60. http://dx.doi.org/10.1016/0041-624x(91)90065-g.

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46

Wei, Dan‐Ping, Dan‐Dan Li, Ai‐Qin Gu, Wen‐Heng Ji, Ying Yang, and Jing‐Pian Peng. "A novel Cytochrome P450 26A1 expressing NK cell subset at the mouse maternal‐foetal interface." Journal of Cellular and Molecular Medicine 25, no. 3 (January 12, 2021): 1771–82. http://dx.doi.org/10.1111/jcmm.16285.

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Burns, Julie E., and Henrik Kacser. "Genetic effects on susceptibility to histidine induced teratogenesis in the mouse." Genetical Research 50, no. 2 (October 1987): 147–53. http://dx.doi.org/10.1017/s0016672300023557.

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SummaryIn the mouse histidinaemia has a teratogenic effect. Animals subjected to high levels of histidine in utero may develop inner ear and behavioural abnormalities typical of the ‘shaker–waltzer’ syndrome. Selection procedures for abnormalities and relaxation of selection have resulted in two histidinaemic strains: the Cambridge strain in which abnormalities occur in over 80% of animals, and the Edinburgh strain in which the penetrance of abnormal behaviour has declined to about 1%. Breeding experiments suggest that the differences are largely due to differences in the genetic backgrounds which modify foetal susceptibilities to the teratogenic effects of high histidine levels. High susceptibility appears to be dominant over low susceptibility in the present strains. There appears to be no interaction of maternal histidinaemia with the dreher mutation which is considered to induce inner ear malformation as a result of an early neural tube abnormality.

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48

Sarraj, M., P. J. McClive, K. L. Loveland, and A. H. Sinclair. "218. Expression of Wsb2 in the mouse testis." Reproduction, Fertility and Development 17, no. 9 (2005): 84. http://dx.doi.org/10.1071/srb05abs218.

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We present a detailed study on the expression pattern of Wsb2 in the mouse foetal and adult gonad. Wsb2 expression was analysed during mouse embryogenesis by whole-mount, section in situ hybridisation and immunohistochemistry. Wsb2 was found to be expressed in the developing mouse gonads from 11.5 dpc to 16.5 dpc. Expression is initially equal in both sexes from 10.5 dpc until 12.0 dpc, then it persists in the male gonad. Wsb2 expression was confined to the cords in both Sertoli cell and germ cells. Other sites of Wsb2 embryonic expression were the somites, dorsal root ganglia and the lateral mantle layer of the neural tube. mRNA encoding Wsb2 and Wsb2 protein has been detected in the newborn testis in both gonocytes and Sertoli cells. Wsb2 mRNA in the adult mouse testis was observed in Sertoli cells, spermatogonia, spermatocytes and the corresponding Wsb2 protein expression was in pachytene spermatocytes, round and elongated spermatids, Sertoli cells and Leydig cells. The differential expression of Wsb2 in male versus female embryonic gonads suggests it may play a role in mammalian sex determination during embryonic development and its expression in the first wave of spermatogenesis and in the adult suggests a later role in spermatogenesis.

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49

Gorošová, A., E. Matalová, I. Kociánová, and F. Tichý. "Langerhans Cells in Feline Foetal Epidermis - Immunohistochemical Study of Spatial Distribution." Acta Veterinaria Brno 77, no. 3 (2008): 307–12. http://dx.doi.org/10.2754/avb200877030307.

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Langerhans cells belong to the skin-associated lymphatic tissue (SALT). They are antigenpresenting cells derived from monocyte precursors in the bone marrow. The distribution of Langerhans cells was investigated in feline foetuses on day 40 of ontogenesis, in 9 selected body regions: regio intermandibularis, regio axilaris, regio prepubica, regio inguinalis, regio parietalis, regio interdigitalis, regio thoracis, regio sacralis and regio caudalis. Mouse monoclonal antibody against CD1 receptor (epitope CD1a) was applied to localize Langerhans cells in the skin samples. The highest number of Langerhans cells was found in biopsy of the dorsal part of the feline foetuses. Langerhans cells were present particularly among keratinocytes of stratum germinativum (stratum basale and stratum spinosum), scattered or clustered among epidermal cells closing the hair canal in the region close to the hair follicle. Langerhans cells were further located among cells of outer root sheath in the region of hair follicle infundibulum close to ostium of sebaceous glands ductus, some were found also in the upper part of the hair follicle isthmus. Langerhans cells seem to participate in skin disorders related to hypersensitivity and even tumour transformations. Distribution of these cells may play a role in disease predispositions; knowledge of the physiology and pathophysiology of Langerhans cells opens possible targeted treatments in veterinary medicine.

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Bird, M. M. "The effects of diethylcarbamazine on the morphology and infrastructure of foetal mouse cerebellar neurons in culture." Journal of Electron Microscopy 49, no. 5 (January 1, 2000): 669–74. http://dx.doi.org/10.1093/oxfordjournals.jmicro.a023857.

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