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Genetics and Molecular Biology of Adipose Cell Characteristics
Published in Claude Bouchard, The Genetics of Obesity, 2020
Gérard P. Ailhaud, Paul A. Grimaldi, Raymond L. Négrel
The process of adipose cell differentiation has been investigated primarily in adipose precursor cells from established clonal lines, such as 3T3-L1, 3T3-F442A, Ob 17, 1246, 3T3-T, and STB, which are all aneuploid. Some investigators have turned to the study of adipose precursor cells derived from the stromal-vascular (SV) fraction of adipose tissues from various species, including humans; these cells are diploid, but have a limited life span. When transplanted into animals, cells from both sources develop into mature © 1994 by CRC Press Inc. 199 fat cells. It is worth pointing out that “differentiation” as applied to adipose precursor cells can have distinct meanings and that this can lead to confusion since, from a developmental perspective, all precursor cells (adipoblasts) are differentiated (or determined) because they are not progenitors of any other cell type. The process of determination (step1, Figure 1) from multipotential stem cells to unipotential adipoblasts cannot be studied easily. However, a determination-like process can be induced by treatment of mouse 10T1/2 and 3T3 cells1 and hamster CHEF-18 cells2 with 5-azacytidine, whereas it is spontaneous in T984 cells isolated from a mouse teratocarcinoma.3 In most cases, these cells are then able to differentiate into adipocytes, chondrocytes, and fibroblasts. Adipose precursor cells or adipoblasts have been cloned from this mixed population of cells.4–6
Cell division
Published in Frank J. Dye, Human Life Before Birth, 2019
Generally, cell division is symmetric; these symmetric cell divisions give rise to daughter cells with the same fates. In times of growth or regeneration, stem cells can also divide symmetrically to produce two identical copies of the original cell. Notably, stem cells may also divide asymmetrically to give rise to two distinct daughter cells: one copy of the original stem cell, as well as a second daughter programmed to differentiate into a non–stem cell fate. Stem cells leave the pool of mitotically dividing cells to begin a process of cell differentiation. Stem cells are, in effect, an embryonic population of cells, continually producing cells that can undergo further development within an adult organism. The path of differentiation that a stem cell descendant enters depends on the molecular environment (niche) in which it resides; for example, erythrocytes, granulocytes, neutrophils, platelets, and lymphocytes shared a common precursor cell, the pluripotential hematopoietic stem cell. See Chapter 6, “Gametogenesis,” for further information on stem cells.
The legal status of the fetus as a patient in Europe
Published in Dagmar Schmitz, Angus Clarke, Wybo Dondorp, The Fetus as a Patient, 2018
Atina Krajewska, Dimitrios Tsarapatsanis
When it comes to the legal status of prenatal human life, it could be particularly important to contrast and compare the position of the ECtHR with the position that the CJEU took in the Brüstle case.32 In Brüstle the CJEU relied on an expansive understanding of human dignity under the Charter of Fundamental Rights to afford a high level of protection to human embryos in vitro. The case concerned the validity of a national German patent regarding the processes for production of neural precursor cells from embryonic stem cells and the use of the former for therapeutic purposes granted to Professor Oliver Brüstle in 1998. The CJEU reasoned that exceptions to patentability pertaining to human embryos had to be interpreted in an expansive way, despite the fact that ‘the definition of human embryo is a very sensitive social issue in many Member States, marked by their multiple traditions and value systems’ (para. 30). It ruled that the concept of human embryo, for the purposes of the ‘bio-patent’ Directive 98/44/EC, must be interpreted broadly as covering any cell capable of commencing the process of development of a human being, including the human ovum as soon as fertilized.
Gene expression profiles and cytokine environments determine the in vitro proliferation and expansion capacities of human hematopoietic stem and progenitor cells
Published in Hematology, 2022
Roberto Dircio-Maldonado, Rosario Castro-Oropeza, Patricia Flores-Guzman, Alberto Cedro-Tanda, Fredy Omar Beltran-Anaya, Alfredo Hidalgo-Miranda, Hector Mayani
In keeping with the above notion and our own results, it has been reported that when the transcriptional profile of CD34+ cells was compared to those of myeloid (myeloblasts) and erythroid (erythroblasts) precursor cells, 47 genes were differentially expressed between CD34+ cells and myeloblasts, in contrast to 492 genes between CD34+ cells and erythroblasts [33]. Interestingly, many of the genes preferentially expressed in myeloblasts (e.g. genes involved in inflammatory response) or erythroblasts (e.g. genes involved in heme biosynthesis and erythrocyte antigens) [34] were not found among the most represented genes observed in MPCs or EPCs (this study). This observation correlates with the more immature stage of the two progenitor cell populations analyzed herein, as compared to morphologically recognizable precursor cells.
Variations in Aspects of Neural Precursor Cell Neurogenesis in a Human Model of HSV-1 Infection
Published in Organogenesis, 2022
Wenxiao Zheng, Emily M. Benner, David C. Bloom, Vaishali Muralidaran, Jill K. Caldwell, Anuya Prabhudesai, Paolo A. Piazza, Joel Wood, Paul R. Kinchington, Vishwajit L. Nimgaonkar, Leonardo D’Aiuto
While HSV-1 is primarily associated with latent infection of peripheral nerve ganglia, it also exhibits a tropism toward the subventricular zone (SVZ) of the lateral ventricles and subgranular zone (SGZ) of the hippocampus.1–4 These regions are particularly enriched with neural stem cells/neural progenitor cells, which play a fundamental role in neurogenesis. We refer to neural stem cells and neural progenitor cells collectively as neural precursor cells (NPCs). Increasing evidence suggests that NPCs themselves are susceptible to HSV-1 in both in vitro and in vivo models.5–8 In general, susceptibility to HSV-1 infection depends on both viral (viral strain, route of infection, and viral dose) and host factors (cell type, strain, and age of the animal). It is not known whether specific cell types from different individuals exhibit comparable infection outcomes. The modeling of the interaction of HSV-1 with NPCs is particularly relevant in relation to the potential mechanistic link between HSV-1 infections and cognition deficits. There is a growing amount of evidence supporting the association of HSV-1 with cognition deficits4, 9–12. Furthermore, in vivo models of HSV-1 infections have shown that viral reactivation in CNS is followed by cognitive deficits.13 A recent study has provided evidence that these cognitive deficits are caused by impaired NPCs neurogenesis in the hippocampus.14
Dendritic Cells Currently under the Spotlight; Classification and Subset Based upon New Markers
Published in Immunological Investigations, 2021
Samaneh Soltani, Mahdi Mahmoudi, Elham Farhadi
The differentiation of DCs is carried out under a highly regulated developmental process from different cell progenitor populations, which are located in bone marrow (Figure 1). DCs live for days or weeks after entering the periphery and should be continually replenished by hematopoiesis (Collin and Bigley 2018). During hematopoiesis, stem cells differentiate into precursor cells that consequently differentiate into more specialized subtypes. In the bone marrow milieu, CD34+ hematopoietic precursors develop to macrophage/DC progenitors (MDPs), which in turn orient to common DC progenitors/precursors (CDPs) that express CD34, CD123, and HLA-DR (Schultze and Aschenbrenner 2019). The CDPs are no longer able to generate monocytes and subsequently restricted to pre–plasmacytoid DCs (pre-pDCs) generation. Pre-pDCs restricted to plasmacytoid (p) DCs or pre-DCs, which differentiate into pre–conventional DCs (pre-cDCs). pre-DCs express CD123, CD303, CD33 (SIGLEC3), CD2, AXL, SIGLEC6 (CD327), CX3 CR1, CD169 (SIGLEC1), CD22 (SIGLEC2). Besides, the expression of Zinc finger E-box-binding homeobox 2 (ZEB2), interferon regulatory factor 4 (IRF4), and Kruppel Like Factor 4 (KLF4) is accepted as their differential transcription factors (TFs) (Collin and Bigley 2018; Schultze and Aschenbrenner 2019).