Journal articles: 'Fetal cell'

1

McCook, Alison. "Fetal Cell Setback." Scientific American 284, no. 5 (May 2001): 25. http://dx.doi.org/10.1038/scientificamerican0501-25c.

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Cassar-Malek, Isabelle, Brigitte Picard, Catherine Jurie, Anne Listrat, Michel Guillomot, Pascale Chavatte-Palmer, and Yvan Heyman. "Myogenesis Is Delayed in Bovine Fetal Clones." Cellular Reprogramming 12, no. 2 (April 2010): 191–201. http://dx.doi.org/10.1089/cell.2009.0065.

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Brodowski, L., B. Schröder-Heurich, C. A. Hubel, T. H. Vu, C. S. von Kaisenberg, and F. von Versen-Höynck. "Role of vitamin D in cell-cell interaction of fetal endothelial progenitor cells and umbilical cord endothelial cells in a preeclampsia-like model." American Journal of Physiology-Cell Physiology 317, no. 2 (August 1, 2019): C348—C357. http://dx.doi.org/10.1152/ajpcell.00109.2019.

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Maternal endothelial dysfunction is a cental feature of preeclampsia (PE), a hypertensive disorder of pregnancy. Factors in the maternal circulation are thought to contribute to this endothelial dysfunction. Although understudied, factors in the fetal circulation may influence fetal endothelial cell interactions with endothelial progenitor cells as critical steps in placental angiogenesis. We hypothesize that cell-cell interactions that are important for pregnancy health are impaired by fetal serum from PE pregnancies and that 1,25(OH)2-vitamin D3 attenuates the negative effects of this serum on cell function. We tested the ability of fetal cord blood-derived endothelial progenitor cells [endothelial colony-forming cells (ECFCs)] to invade into established monolayers and capillary tubule-like structures of human fetal umbilical venous endothelial cells (HUVECs), while in the presence/absence of fetal cord serum from uncomplicated or PE pregnancies, and tested the ability of 1,25(OH)2-vitamin D3 to modulate the serum-mediated effects. PE cord serum reduced the invasion of fetal ECFCs into HUVEC monolayers or tubule networks. Vitamin D attenuated these effects of PE fetal serum on endothelial functional properties. Immunocytochemical studies revealed involvement of VE-cadherin contacts in interactions between ECFCs and mature fetal endothelial cells. PE cord serum reduces the ability of fetal endothelial progenitor cells to incorporate into fetal endothelial cell networks. Physiologic concentrations of vitamin D reverse these PE serum-mediated effects. These data appear consistent with lines of evidence that vitamin D has antipreeclampsia effects.

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KATLAN, Doruk Cevdi, and Feride SÖYLEMEZ. "Cell-Free Fetal DNA in Prenatal Screening." Turkiye Klinikleri Journal of Health Sciences 2, no. 3 (2017): 165–73. http://dx.doi.org/10.5336/healthsci.2016-51564.

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5

Kearney, J., F. Martin, C. Benedict, and A. Oliver. "Fetal B cell development." Immunology Letters 56 (May 1997): 98. http://dx.doi.org/10.1016/s0165-2478(97)85389-8.

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Kearney, J. "Fetal B cell development." Immunology Letters 56, no. 1-3 (May 1997): 98. http://dx.doi.org/10.1016/s0165-2478(97)87227-6.

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7

Tiblad, Eleonor, and Magnus Westgren. "Fetal stem-cell transplantation." Best Practice & Research Clinical Obstetrics & Gynaecology 22, no. 1 (February 2008): 189–201. http://dx.doi.org/10.1016/j.bpobgyn.2007.07.007.

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8

Frost, Mackenzie S., Aqib H. Zehri, Sean W. Limesand, William W. Hay, and Paul J. Rozance. "Differential Effects of Chronic Pulsatile versus Chronic Constant Maternal Hyperglycemia on Fetal Pancreaticβ-Cells." Journal of Pregnancy 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/812094.

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Constant maternal hyperglycemia limits, while pulsatile maternal hyperglycemia may enhance, fetal glucose-stimulated insulin secretion (GSIS) in sheep. However, the impact of such different patterns of hyperglycemia on the development of the fetalβ-cell is unknown. We measured the impact of one week of chronic constant hyperglycemia (CHG,n=6) versus pulsatile hyperglycemia (PHG,n=5) versus controls (n=7) on the percentage of the fetal pancreas staining for insulin (β-cell area), mitotic and apoptotic indices and size of fetalβ-cells, and fetal insulin secretion in sheep. Baseline insulin concentrations were higher in CHG fetuses (P<0.05) compared to controls and PHG. GSIS was lower in the CHG group (P<0.005) compared to controls and PHG. PHGβ-cell area was increased 50% (P<0.05) compared to controls and CHG. CHGβ-cell apoptosis was increased over 400% (P<0.05) compared to controls and PHG. These results indicate that late gestation constant maternal hyperglycemia leads to significantβ-cell toxicity (increased apoptosis and decreased GSIS). Furthermore, pulsatile maternal hyperglycemia increases pancreaticβ-cell area but did not increase GSIS, indicating decreasedβ-cell responsiveness. These findings demonstrate differential effects that the pattern of maternal hyperglycemia has on fetal pancreaticβ-cell development, which might contribute to later life limitation in insulin secretion.

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Zhao, Xiao Xi, Nobuhiro Suzumori, Yasuhiko Ozaki, Takeshi Sato, and Kaoru Suzumori. "Examination of Fetal Cells and Cell-Free Fetal DNA in Maternal Blood for Fetal Gender Determination." Gynecologic and Obstetric Investigation 58, no. 1 (2004): 57–60. http://dx.doi.org/10.1159/000078577.

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10

Ng, Melissa, Theodore Roth, Ventura Mendoza, Alexander Marson, and Trevor Burt. "Helios predisposes human fetal CD4+ naive T cells towards regulatory T cell differentiation." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 124.9. http://dx.doi.org/10.4049/jimmunol.202.supp.124.9.

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Abstract Activation of naïve CD4+ T cells by T cell receptor (TCR) stimulation and cytokine cues lead to differentiation into effector T cell populations with distinct pro-inflammatory or regulatory functions. Unlike adult naïve T cells, human fetal naïve CD4+ T cells uniquely differentiate into FOXP3+ regulatory T (Treg) cells upon TCR activation independent of exogenous cytokine signalling. This facility for Treg differentiation is crucial for generating tolerance in utero; however, the mechanisms underlying this ability in fetal naïve cells are largely unknown. Here, we reveal FOXP3-independent transcriptional and epigenetic programs shared between fetal naive T cells and committed adult Treg cells that are inactive in adult naive T cells. We show that a subset of adult Treg-specific super-enhancers is active within fetal naive T cells, including two super-enhancers at Helios, a thymic Treg gene. Helios is expressed in fetal naive T cells, but not in adult naïve T cells, and only fetal-derived induced Treg (iTreg) cells continue to express Helios. Fetal, but not adult iTreg cells, have suppressed IL-2 production, which is regulated by Helios in committed Treg cells. CRISPR-Cas9 ablation of Helios in fetal naive T cells then resulted in increased IL-2 production in fetal iTreg cells. Crucially, the loss of Helios expression in fetal naïve T cells impaired their differentiation into Treg cells upon TCR stimulation, indicating Helios as a critical contributor to the cell-intrinsic predisposition of fetal naive T cells for Treg cell differentiation. Treg-biased transcriptional and epigenetic programs within fetal naive T cells identified here could be utilized to engineer enhanced adult iTreg populations for adoptive cellular therapies.

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11

Thomson, Alison J., Hadrien Pierart, Stephen Meek, Alexandra Bogerman, Linda Sutherland, Helen Murray, Edward Mountjoy, et al. "Reprogramming Pig Fetal Fibroblasts Reveals a Functional LIF Signaling Pathway." Cellular Reprogramming 14, no. 2 (April 2012): 112–22. http://dx.doi.org/10.1089/cell.2011.0078.

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12

Wen, Qing, Yuqian Wang, Jixin Tang, C. Yan Cheng, and Yi-Xun Liu. "Sertoli Cell Wt1 Regulates Peritubular Myoid Cell and Fetal Leydig Cell Differentiation during Fetal Testis Development." PLOS ONE 11, no. 12 (December 30, 2016): e0167920. http://dx.doi.org/10.1371/journal.pone.0167920.

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Barsoum, I. B., and H. H. C. Yao. "Fetal Leydig Cells: Progenitor Cell Maintenance and Differentiation." Journal of Andrology 31, no. 1 (October 29, 2009): 11–15. http://dx.doi.org/10.2164/jandrol.109.008318.

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14

Rosner, Margit, and Markus Hengstschläger. "Amniotic fluid stem cells and fetal cell microchimerism." Trends in Molecular Medicine 19, no. 5 (May 2013): 271–72. http://dx.doi.org/10.1016/j.molmed.2013.01.001.

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15

Zhou, Kun, Caihong Hu, Zhigang Zhou, Lifang Huang, Wenli Liu, and Hanying Sun. "Fetal liver stromal cells promote hematopoietic cell expansion." Biochemical and Biophysical Research Communications 387, no. 3 (September 2009): 596–601. http://dx.doi.org/10.1016/j.bbrc.2009.07.071.

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16

McDougall, Annie R. A., Stuart B. Hooper, Valerie A. Zahra, Foula Sozo, Camden Y. Lo, Timothy J. Cole, Tim Doran, and Megan J. Wallace. "The oncogeneTrop2regulates fetal lung cell proliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 4 (October 2011): L478—L489. http://dx.doi.org/10.1152/ajplung.00063.2011.

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The factors regulating growth of the developing lung are poorly understood, although the degree of fetal lung expansion is critical. The oncogene Trop2 (trophoblast antigen 2) is upregulated during accelerated fetal lung growth, and we hypothesized that it may regulate normal fetal lung growth. We investigated Trop2 expression in the fetal and neonatal sheep lung during accelerated and delayed lung growth induced by alterations in fetal lung expansion, as well as in response to glucocorticoids. Trop2 expression was measured using real-time PCR and localized spatially using in situ hybridization and immunofluorescence. During normal lung development, Trop2 expression was higher at 90 days gestational age (GA; 4.0 ± 0.8) than at 128 days GA (1.0 ± 0.1), decreased to 0.5 ± 0.1 at 142 days GA (full term ∼147 days GA), and was positively correlated to lung cell proliferation rates ( r = 0.953, P < 0.005). Trop2 expression was regulated by fetal lung expansion, but not by glucocorticoids. It was increased nearly threefold by 36 h of increased fetal lung expansion ( P < 0.05) and was reduced to ∼55% of control levels by reduced fetal lung expansion ( P < 0.05). Trop2 expression was associated with lung cell proliferation during normal and altered lung growth, and the TROP2 protein colocalized with Ki-67-positive cells in the fetal lung. TROP2 was predominantly localized to fibroblasts and type II alveolar epithelial cells. Trop2 small interfering RNA decreased Trop2 expression by ∼75% in cultured fetal rat lung fibroblasts and decreased their proliferation by ∼50%. Cell viability was not affected. This study demonstrates that TROP2 regulates lung cell proliferation during development.

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17

Weiss, R. "Human Fetal-Cell Transplants Planned." Science News 132, no. 2 (July 11, 1987): 22. http://dx.doi.org/10.2307/3971772.

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18

Shaaban, Aimen F., and Alan W. Flake. "Fetal hematopoietic stem cell transplantation." Seminars in Perinatology 23, no. 6 (December 1999): 515–23. http://dx.doi.org/10.1016/s0146-0005(99)80030-5.

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19

Coles, Peter. "French fetal cell transplant operations." Nature 348, no. 6303 (December 1990): 667. http://dx.doi.org/10.1038/348667b0.

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20

Abbott, Alison. "Fetal-cell revival for Parkinson’s." Nature 510, no. 7504 (June 2014): 195–96. http://dx.doi.org/10.1038/510195a.

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21

Everett, T. R., and L. S. Chitty. "Cell-free fetal DNA: the new tool in fetal medicine." Ultrasound in Obstetrics & Gynecology 45, no. 5 (April 24, 2015): 499–507. http://dx.doi.org/10.1002/uog.14746.

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22

Shafritz, David A., Mo R. Ebrahimkhani, and Michael Oertel. "Therapeutic Cell Repopulation of the Liver: From Fetal Rat Cells to Synthetic Human Tissues." Cells 12, no. 4 (February 6, 2023): 529. http://dx.doi.org/10.3390/cells12040529.

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Progenitor cells isolated from the fetal liver can provide a unique cell source to generate new healthy tissue mass. Almost 20 years ago, it was demonstrated that rat fetal liver cells repopulate the normal host liver environment via a mechanism akin to cell competition. Activin A, which is produced by hepatocytes, was identified as an important player during cell competition. Because of reduced activin receptor expression, highly proliferative fetal liver stem/progenitor cells are resistant to activin A and therefore exhibit a growth advantage compared to hepatocytes. As a result, transplanted fetal liver cells are capable of repopulating normal livers. Important for cell-based therapies, hepatic stem/progenitor cells containing repopulation potential can be separated from fetal hematopoietic cells using the cell surface marker δ-like 1 (Dlk-1). In livers with advanced fibrosis, fetal epithelial stem/progenitor cells differentiate into functional hepatic cells and out-compete injured endogenous hepatocytes, which cause anti-fibrotic effects. Although fetal liver cells efficiently repopulate the liver, they will likely not be used for human cell transplantation. Thus, utilizing the underlying mechanism of repopulation and developed methods to produce similar growth-advantaged cells in vitro, such as human induced pluripotent stem cells (iPSCs). This approach has great translational potential for developing novel cell-based therapies in patients with liver disease. The present review gives a brief overview of the classic cell transplantation models and various cell sources studied as donor cell candidates. The advantages of fetal liver-derived stem/progenitor cells are discussed, as well as the mechanism of liver repopulation. Moreover, this article reviews the potential of in vitro developed synthetic human fetal livers from iPSCs and their therapeutic benefits.

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23

Adkins, B., and K. Hamilton. "Developmental ages of the thymic epithelium and of the T cell precursors together determine the proportions of peripheral CD4+ cells." Journal of Immunology 153, no. 12 (December 15, 1994): 5359–65. http://dx.doi.org/10.4049/jimmunol.153.12.5359.

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Abstract In earlier studies on chimeric animals, we found that fetal thymocytes produced peripheral T lymphocyte populations depleted of CD4+ cells. This occurred whether the fetal thymocytes matured in the presence of adult or fetal thymic stromal cells. In contrast, fetal liver cells that differentiated in the adult thymus generated normal proportions of peripheral CD4+ cells. Because fetal liver cells are thought to be the immediate precursors to fetal thymocytes, we proposed that fetal thymic stroma would modulate the differentiation of fetal liver cells; specifically, that fetal liver cells maturing in the fetal thymus would resemble fetal thymocytes and produce low levels of peripheral CD4+ cells. To test this hypothesis, fetal thymic lobes were colonized in vitro with fetal liver cells and subsequently transplanted in vivo to Thy-1 congenic hosts. Under these conditions, fetal liver cells produced reduced proportions of CD4+ peripheral progeny. The under-representation of CD4+ peripheral T cells was apparently governed by the thymic epithelium because similar results were obtained with 2-deoxyguanosine-treated fetal thymuses colonized by fetal liver cells. In contrast, adult bone marrow cells made normal levels of CD4+ peripheral T cells whether maturation occurred in the fetal or the adult thymus. Thus, pre-T cells (fetal liver or adult bone marrow) lose the capacity to respond to fetal thymic stromal cells during development. These results indicate that the proportions of CD4+ cells in peripheral tissues are regulated by a combination of the developmental ages of the T cell precursors and the thymic stromal environment.

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24

Padron, Justin Gary, Nainoa D. Norman Ing, Po’okela K. Ng, and Claire E. Kendal-Wright. "Stretch Causes Cell Stress and the Downregulation of Nrf2 in Primary Amnion Cells." Biomolecules 12, no. 6 (May 31, 2022): 766. http://dx.doi.org/10.3390/biom12060766.

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Nuclear-factor-E2-related factor 2 (Nrf2) is a key transcription factor for the regulation of cellular responses to cellular stress and inflammation, and its expression is significantly lower after spontaneous term labor in human fetal membranes. Pathological induction of inflammation can lead to adverse pregnancy outcomes such as pre-eclampsia, preterm labor, and fetal death. As stretch forces are known to act upon the fetal membranes in utero, we aimed to ascertain the effect of stretch on Nrf2 to increase our understanding of the role of this stimulus on cells of the amnion at term. Our results indicated a significant reduction in Nrf2 expression in stretched isolated human amnion epithelial cells (hAECs) that could be rescued with sulforaphane treatment. Downregulation of Nrf2 as a result of stretch was accompanied with activation of proinflammatory nuclear factor-kB (NF-kB) and increases in LDH activity, ROS, and HMGB1. This work supports stretch as a key modulator of cellular stress and inflammation in the fetal membranes. Our results showed that the modulation of the antioxidant response pathway in the fetal membranes through Nrf2 activation may be a viable approach to improve outcomes in pregnancy.

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25

GOWRI, A. MANGALA. "FETAL MESENCHYMAL STEM CELL BIO MARKING FOR TRACKING CELLS." IOSR Journal of Pharmacy (IOSRPHR) 2, no. 2 (January 2012): 342–44. http://dx.doi.org/10.9790/3013-0220342344.

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26

CANIGGIA, I., and M. POST. "Glycosaminoglycan synthesis by fetal lung cells: Cell-matrix interactions." Cell Biology International Reports 14 (September 1990): 125. http://dx.doi.org/10.1016/0309-1651(90)90600-4.

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27

Jotereau, F., F. Heuze, V. Salomon-Vie, and H. Gascan. "Cell kinetics in the fetal mouse thymus: precursor cell input, proliferation, and emigration." Journal of Immunology 138, no. 4 (February 15, 1987): 1026–30. http://dx.doi.org/10.4049/jimmunol.138.4.1026.

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Abstract The entry and differentiation of lymphoid precursor cells (LPC) in grafted mouse fetal thymuses and the emigration of explants thymocytes has been followed in a system in which donor and host lymphocytes could be distinguished on the basis of Thy-1 expression. It appears that LPC that invade the fetal mouse thymus between 10 and 13 days rapidly differentiate into Thy-1 positive thymocytes, giving rise to all of the lymphoid populations of both cortical and medullary locations until approximately the end of the first week after birth. Lymphoid precursor cells that enter the fetal thymus after 13 days of fetal life only differentiate into Thy-1 positive lymphocytes 6 or 7 days after birth, when they give rise to a second generation of thymocytes that grows exponentially and completely replaces the first generation in approximately 8 days. All cells leaving the thymus during the first 2 wk of life appear to be derived from the first wave of precursors.

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28

Guo, Zengli, Wei-Chun Chou, Gang Wang, and Yisong Y. Wan. "Missing link in human fetal immunity: fetal dendritic cells orchestrate prenatal T cell immune suppression." AME Medical Journal 2 (October 2017): 152. http://dx.doi.org/10.21037/amj.2017.09.11.

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29

Hahn, S. "Fetal cells and cell-free fetal DNA in maternal blood: new insights into pre-eclampsia." Human Reproduction Update 8, no. 6 (November 1, 2002): 501–8. http://dx.doi.org/10.1093/humupd/8.6.501.

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30

Bianchi, Diana W. "Fetal cells in the mother: from genetic diagnosis to diseases associated with fetal cell microchimerism." European Journal of Obstetrics & Gynecology and Reproductive Biology 92, no. 1 (September 2000): 103–8. http://dx.doi.org/10.1016/s0301-2115(00)00432-2.

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31

de Leon, Priscila Marques Moura, Vinicius Farias Campos, Odir Antônio Dellagostin, João Carlos Deschamps, Fabiana Kömmling Seixas, and Tiago Collares. "Equine fetal sex determination using circulating cell-free fetal DNA (ccffDNA)." Theriogenology 77, no. 3 (February 2012): 694–98. http://dx.doi.org/10.1016/j.theriogenology.2011.09.005.

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32

Gunji, Y., T. Sudo, J. Suda, Y. Yamaguchi, H. Nakauchi, S. Nishikawa, N. Yanai, M. Obinata, M. Yanagisawa, and Y. Miura. "Support of early B-cell differentiation in mouse fetal liver by stromal cells and interleukin-7." Blood 77, no. 12 (June 15, 1991): 2612–17. http://dx.doi.org/10.1182/blood.v77.12.2612.2612.

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Abstract We compared the development of B-cell progenitors with that of myeloid progenitors in fetal liver cells at various gestational ages. Day 12 to 14 fetal liver cells did not form pre-B-cell colonies. Pre-B-cell colonies were developed from day 15 fetal liver cells. The incidence of colonies increased with increases in gestational age and reached a maximum on days 18 to 19. In contrast, the incidence of myeloid colonies formed in the presence of interleukin-3 (IL-3) and erythropoietin did not change significantly during days 13 to 21 of gestation. After coculturing day 13 fetal liver cells with IL-7- producing stromal cell line ST-2, they could respond to IL-7 and proliferate. Analysis of the phenotypes showed that day 13 fetal liver cells were B220-, IgM-, while culturing day 13 fetal liver cells with ST-2 and untreated day 18 fetal liver cells contained the population of B220+ cells. Even in the presence of IL-7-defective stromal cell line FLS-3, IL-7-responsive cells could be induced from day 13 fetal liver cells. IL-7 acted on B220+ cells and induced pre-B-cell colonies that contained IgM+ cells in the methylcellulose culture. IL-7 mRNA was expressed in days 13 and 18 fetal liver cells but not in pre-B cells or adult liver cells. From these findings, it is suggested that stromal cells or stromal-derived factors but not IL-7 were required for the differentiation from B220- cells to B220+ cells. In the second stage, B220+, IgM- cells proliferated and some of them differentiated to IgM+ cells in the presence of IL-7 alone. The two-step model can apply to in vivo early B lymphopoiesis.

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Gunji, Y., T. Sudo, J. Suda, Y. Yamaguchi, H. Nakauchi, S. Nishikawa, N. Yanai, M. Obinata, M. Yanagisawa, and Y. Miura. "Support of early B-cell differentiation in mouse fetal liver by stromal cells and interleukin-7." Blood 77, no. 12 (June 15, 1991): 2612–17. http://dx.doi.org/10.1182/blood.v77.12.2612.bloodjournal77122612.

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We compared the development of B-cell progenitors with that of myeloid progenitors in fetal liver cells at various gestational ages. Day 12 to 14 fetal liver cells did not form pre-B-cell colonies. Pre-B-cell colonies were developed from day 15 fetal liver cells. The incidence of colonies increased with increases in gestational age and reached a maximum on days 18 to 19. In contrast, the incidence of myeloid colonies formed in the presence of interleukin-3 (IL-3) and erythropoietin did not change significantly during days 13 to 21 of gestation. After coculturing day 13 fetal liver cells with IL-7- producing stromal cell line ST-2, they could respond to IL-7 and proliferate. Analysis of the phenotypes showed that day 13 fetal liver cells were B220-, IgM-, while culturing day 13 fetal liver cells with ST-2 and untreated day 18 fetal liver cells contained the population of B220+ cells. Even in the presence of IL-7-defective stromal cell line FLS-3, IL-7-responsive cells could be induced from day 13 fetal liver cells. IL-7 acted on B220+ cells and induced pre-B-cell colonies that contained IgM+ cells in the methylcellulose culture. IL-7 mRNA was expressed in days 13 and 18 fetal liver cells but not in pre-B cells or adult liver cells. From these findings, it is suggested that stromal cells or stromal-derived factors but not IL-7 were required for the differentiation from B220- cells to B220+ cells. In the second stage, B220+, IgM- cells proliferated and some of them differentiated to IgM+ cells in the presence of IL-7 alone. The two-step model can apply to in vivo early B lymphopoiesis.

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34

Tang, Yanjuan, Claudia Peitzsch, Hojjatollah Nozad Charoudeh, Min Cheng, Patricia Chaves, Sten Eirik W. Jacobsen, and Ewa Sitnicka. "Emergence of NK-cell progenitors and functionally competent NK-cell lineage subsets in the early mouse embryo." Blood 120, no. 1 (July 5, 2012): 63–75. http://dx.doi.org/10.1182/blood-2011-02-337980.

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Abstract The earliest stages of natural killer (NK)–cell development are not well characterized. In this study, we investigated in different fetal hematopoietic tissues how NK-cell progenitors and their mature NK-cell progeny emerge and expand during fetal development. Here we demonstrate, for the first time, that the counterpart of adult BM Lin−CD122+NK1.1−DX5− NK-cell progenitor (NKP) emerges in the fetal liver at E13.5. After NKP expansion, immature NK cells emerge at E14.5 in the liver and E15.5 in the spleen. Thymic NK cells arise at E15.5, whereas functionally competent cytotoxic NK cells were present in the liver and spleen at E16.5 and E17.5, respectively. Fetal NKPs failed to produce B and myeloid cells but sustained combined NK- and T-lineage potential at the single-cell level. NKPs were also found in the fetal blood, spleen, and thymus. These findings show the emergence and expansion of bipotent NK/T-cell progenitor during fetal and adult lymphopoiesis, further supporting that NK/T-lineage restriction is taking place prethymically. Uncovering the earliest NK-cell developmental stages will provide important clues, helping to understand the origin of diverse NK-cell subsets, their progenitors, and key regulators.

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Tu, Jian, and Bernard E. Tuch. "Expression of Glucokinase in Glucose-Unresponsive Human Fetal Pancreatic Islet-Like Cell Clusters1." Journal of Clinical Endocrinology & Metabolism 82, no. 3 (March 1, 1997): 943–48. http://dx.doi.org/10.1210/jcem.82.3.3837.

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Abstract Glucokinase (GK) is the glucose sensor in the adult β-cell, resulting in fuel for insulin synthesis and secretion. Defects in this enzyme in the β-cell are responsible for the genetic disorder maturity-onset diabetes of the young, with the β-cell being unable to secrete insulin appropriately when challenged with glucose. The human fetalβ -cell is also unable to secrete insulin when exposed to glucose, but whether GK is present and functional in this developing cell is unknown. To determine the expression of GK in human fetal pancreatic tissue, cytosolic protein was extracted from human fetal islet-like cell clusters (ICCs) at 17–19 weeks gestation and examined for protein content and enzyme activity. On Western blots, a single band corresponding to GK was seen at 52 kDa, and this was similar to that obtained from human adult islets. The maximal velocity (Vmax) of GK was less in fetal ICCs than that in adult islets (8.7 vs. 20.7 nmol/mg protein·h); similar Km values were found in both ICCs and islets. No attempt was made to determine which cells in an ICC contained GK. Glucose utilization was determined radiometrically; the Vmax of the high Km component was less in ICCs than in islets (31.3 pmol/ICC·h vs. 101.4 pmol/islet·h). Culture of ICCs for 3–7 days in medium containing 11.2 mmol/L glucose resulted in a 3.7-fold increase in the Vmax of GK and a 1.8-fold increase in glucose utilization. These enhanced activities of glucose phosphorylation and glycolysis, however, did not lead to the β-cell being able to secrete insulin when exposed to glucose. In conclusion, glucokinase is present and functional in human fetal ICCs, but the inability of the human fetal β-cell to secrete insulin in response to an acute glucose challenge is not due to immaturity of this enzyme.

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Liu, Fei, Jae Y. Lee, Huijun Wei, Osamu Tanabe, James D. Engel, Sean J. Morrison, and Jun-Lin Guan. "FIP200 is required for the cell-autonomous maintenance of fetal hematopoietic stem cells." Blood 116, no. 23 (December 2, 2010): 4806–14. http://dx.doi.org/10.1182/blood-2010-06-288589.

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Abstract Little is known about whether autophagic mechanisms are active in hematopoietic stem cells (HSCs) or how they are regulated. FIP200 (200-kDa FAK-family interacting protein) plays important roles in mammalian autophagy and other cellular functions, but its role in hematopoietic cells has not been examined. Here we show that conditional deletion of FIP200 in hematopoietic cells leads to perinatal lethality and severe anemia. FIP200 was cell-autonomously required for the maintenance and function of fetal HSCs. FIP200-deficient HSC were unable to reconstitute lethally irradiated recipients. FIP200 ablation did not result in increased HSC apoptosis, but it did increase the rate of HSC proliferation. Consistent with an essential role for FIP200 in autophagy, FIP200-null fetal HSCs exhibited both increased mitochondrial mass and reactive oxygen species. These data identify FIP200 as a key intrinsic regulator of fetal HSCs and implicate a potential role for autophagy in the maintenance of fetal hematopoiesis and HSCs.

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37

Adkins, B. "Developmental regulation of the intrathymic T cell precursor population." Journal of Immunology 146, no. 5 (March 1, 1991): 1387–93. http://dx.doi.org/10.4049/jimmunol.146.5.1387.

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Abstract The maturation potential of CD4-8- thymocytes purified from mice of different developmental ages was examined in vivo after intrathymic injection. As previously reported, 14-day fetal CD4-8- thymocytes produced fewer CD4+ than CD8+ progeny in peripheral lymphoid tissues, resulting in a CD4+:CD8+ ratio of less than or equal to 1.0. In contrast, adult CD4-8- thymocytes generated CD4+ or CD8+ peripheral progeny in the proportions found in the normal adult animal (CD4+:CD8+ = 2 to 3). Here we have shown that CD4-8- precursor cells from the 17-day fetal thymus also produced peripheral lymphocytes with low CD4+:CD8+ ratios. Precursors from full term fetuses produced slightly higher CD4+:CD8+ ratios (1.1-1.6) and precursors from animals three to 4 days post-birth achieved CD4+:CD8+ ratios intermediate between those produced by fetal and adult CD4-8- thymocytes. Parallel changes in the production of alpha beta TCR+ peripheral progeny were observed. Fetal CD4-8- thymocytes generated fewer alpha beta TCR+ progeny than did adult CD4-8- thymocytes. However, peripheral lymphocytes arising from either fetal or adult thymic precursors showed similar proportions of gamma delta TCR+ cells. The same pattern of progeny was observed when fetal CD4-8- thymocytes matured in an adult or in a fetal thymic stromal environment. In contrast to fetal thymic precursors, fetal liver T cell precursors resembled adult CD4-8- thymocytes by all parameters measured. These results suggest that fetal thymic precursors are intrinsically different from both adult CD4-8- thymocytes and fetal liver T cell precursors. Moreover, they lead to the hypothesis that the composition of the peripheral T cell compartment is developmentally regulated by the types of precursors found in the thymus. A model is proposed in which migration of adult-like precursors from the fetal liver to the thymus approximately at birth triggers a transition from the fetal to the adult stages of intrathymic T cell differentiation.

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Haynes, B. F., M. E. Martin, H. H. Kay, and J. Kurtzberg. "Early events in human T cell ontogeny. Phenotypic characterization and immunohistologic localization of T cell precursors in early human fetal tissues." Journal of Experimental Medicine 168, no. 3 (September 1, 1988): 1061–80. http://dx.doi.org/10.1084/jem.168.3.1061.

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During early fetal development, T cell precursors home from fetal yolk sac and liver to the epithelial thymic rudiment. From cells that initially colonize the thymus arise mature T cells that populate T cell zones of the peripheral lymphoid system. Whereas colonization of the thymus occurs late in the final third of gestation in the mouse, in birds and humans the thymus is colonized by hematopoietic stem cell precursors during the first third of gestation. Using a large series of early human fetal tissues and a panel of monoclonal antibodies that includes markers of early T cells (CD7, CD45), we have studied the immunohistologic location and differentiation capacity of CD45+, CD7+ cells in human fetal tissues. We found that before T cell precursor colonization of the thymus (7-8 wk of gestation), CD7+ cells were present in yolk sac, neck, upper thorax, and fetal liver, and were concentrated in mesenchyme throughout the upper thorax and neck areas. By 9.5 wk of gestation, CD7+ cells were no longer present in upper thorax mesenchyme but rather were localized in the lymphoid thymus and scattered throughout fetal liver. CD7+, CD2-, CD3-, CD8-, CD4-, WT31- cells in thorax and fetal liver, when stimulated for 10-15 d with T cell-conditioned media and rIL-2, expressed CD2, CD3, CD4, CD8, and WT31 markers of the T cell lineage. Moreover, CD7+ cells isolated from fetal liver contained all cells in this tissue capable of forming CFU-T colonies in vitro. These data demonstrate that T cell precursors in early human fetal tissues can be identified using a mAb against the CD7 antigen. Moreover, the localization of CD7+ T cell precursors to fetal upper thorax and neck areas at 7-8.5 wk of fetal gestation provides strong evidence for a developmentally regulated period in man in which T cell precursors migrate to the epithelial thymic rudiment.

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Rivera, Alicia. "Sickle cell disease and fetal hemoglobin." Saudi Journal of Medicine and Medical Sciences 6, no. 3 (2018): 131. http://dx.doi.org/10.4103/sjmms.sjmms_128_18.

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40

Weiss, R. "Fetal-Cell Transplants Put on Hold." Science News 133, no. 17 (April 23, 1988): 260. http://dx.doi.org/10.2307/3972443.

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41

Weiss, R. "Fetal-Cell Transplants Show Few Benefits." Science News 134, no. 21 (November 19, 1988): 324. http://dx.doi.org/10.2307/3972903.

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Weiss, Rick. "Forbidding Fruits of Fetal-Cell Research." Science News 134, no. 19 (November 5, 1988): 296. http://dx.doi.org/10.2307/3973073.

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Samuelsen, Grethe Badsberg, Nenad Bogdanović, Henning Laursen, Niels Graem, Jørgen Falck Larsen, and Bente Pakkenberg. "TOTAL CELL NUMBER IN FETAL BRAIN." Image Analysis & Stereology 19, no. 1 (May 3, 2011): 35. http://dx.doi.org/10.5566/ias.v19.p35-38.

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In this study the material comprises brains from three aborted fetuses and two fullterm infants who died at birth.The gestational ages ranged from the 22nd week to term. All cases were without malformations, known chromosomal abnormality, hydrops, and systemic infections, and all had normal birth weights with fetal growth indices (observed birth weight/expected mean birth weight) between 0.9 - 1.05. The preliminary results show a five fold increase in the total cell population in the marginal zone/cortical plate, MZ/CP (future neocortex), from week 22 until term. In the transient subplate zone, SP, the total cell number was more than doubled from week 22 to week 30-35, and then decreased towards term. In the intermediate zone, IZ (future white matter), the total cell population was doubled from week 22 until term. The total cell number in the entricular/subventricular zone, VZ/SZ (germinal matrix), was reduced by a factor of five from week 22 until term. A histological differentiation between neurons and glial cells was not possible. The optical fractionator was used to estimate the total cell population in four characteristic developmental zones in the human fetal brain. Fetal brain tissue undergoes considerable and rather unpredictable shrinkage during fixation. However, using the fractionator principle it is possible to eliminate this problem, provided that the structure of interest (one brain hemisphere) is fully intact.

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Pilones, Karsten, Zhi-Wei Lai, and Jerrie Gavalchin. "Prenatal HgCl2Exposure Alters Fetal Cell Phenotypes." Journal of Immunotoxicology 4, no. 4 (January 2007): 295–301. http://dx.doi.org/10.1080/15476910701680178.

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Merchant, F. A. "Strategies for automated fetal cell screening." Human Reproduction Update 8, no. 6 (November 1, 2002): 509–21. http://dx.doi.org/10.1093/humupd/8.6.509.

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Steinberg, Martin H. "Fetal hemoglobin in sickle cell anemia." Blood 136, no. 21 (November 19, 2020): 2392–400. http://dx.doi.org/10.1182/blood.2020007645.

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Abstract Fetal hemoglobin (HbF) can blunt the pathophysiology, temper the clinical course, and offer prospects for curative therapy of sickle cell disease. This review focuses on (1) HbF quantitative trait loci and the geography of β-globin gene haplotypes, especially those found in the Middle East; (2) how HbF might differentially impact the pathophysiology and many subphenotypes of sickle cell disease; (3) clinical implications of person-to-person variation in the distribution of HbF among HbF-containing erythrocytes; and (4) reactivation of HbF gene expression using both pharmacologic and cell-based therapeutic approaches. A confluence of detailed understanding of the molecular basis of HbF gene expression, coupled with the ability to precisely target by genomic editing most areas of the genome, is producing important preliminary therapeutic results that could provide new options for cell-based therapeutics with curative intent.

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Akinsheye, Idowu, Abdulrahman Alsultan, Nadia Solovieff, Duyen Ngo, Clinton T. Baldwin, Paola Sebastiani, David H. K. Chui, and Martin H. Steinberg. "Fetal hemoglobin in sickle cell anemia." Blood 118, no. 1 (July 7, 2011): 19–27. http://dx.doi.org/10.1182/blood-2011-03-325258.

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Abstract Fetal hemoglobin (HbF) is the major genetic modulator of the hematologic and clinical features of sickle cell disease, an effect mediated by its exclusion from the sickle hemoglobin polymer. Fetal hemoglobin genes are genetically regulated, and the level of HbF and its distribution among sickle erythrocytes is highly variable. Some patients with sickle cell disease have exceptionally high levels of HbF that are associated with the Senegal and Saudi-Indian haplotype of the HBB-like gene cluster; some patients with different haplotypes can have similarly high HbF. In these patients, high HbF is associated with generally milder but not asymptomatic disease. Studying these persons might provide additional insights into HbF gene regulation. HbF appears to benefit some complications of disease more than others. This might be related to the premature destruction of erythrocytes that do not contain HbF, even though the total HbF concentration is high. Recent insights into HbF regulation have spurred new efforts to induce high HbF levels in sickle cell disease beyond those achievable with the current limited repertory of HbF inducers.

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Touraine, Jean-Louis. "Perinatal fetal-cell and gene therapy." International Journal of Immunopharmacology 22, no. 12 (December 2000): 1033–40. http://dx.doi.org/10.1016/s0192-0561(00)00076-x.

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Frazier, A. Lindsay, Christopher Weldon, and James Amatruda. "Fetal and neonatal germ cell tumors." Seminars in Fetal and Neonatal Medicine 17, no. 4 (August 2012): 222–30. http://dx.doi.org/10.1016/j.siny.2012.05.004.

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Witt, Russell, Tippi C. MacKenzie, and William H. Peranteau. "Fetal stem cell and gene therapy." Seminars in Fetal and Neonatal Medicine 22, no. 6 (December 2017): 410–14. http://dx.doi.org/10.1016/j.siny.2017.05.003.

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Journal articles on the topic 'Fetal cell'

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