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Stimulation of Pluripotent Hematopoietic Stem Cell by Growth Factors Released by Malignant
Published in Velibor Krsmanović, James F. Whitfield, Malignant Cell Secretion, 2019
The first hematopoietic cell to fulfill these criteria was the pluripotent stem cell, CFU-S (colony forming-cell in the spleen), described in 1961 by Till and McCulloch.22 By injecting a marrow suspension into lethally irradiated mice, they observed the occurrence, 9 d later, of small nodules at the surface of the spleen, each of which originated from a single cell. This assay, which is not feasible in humans, has been widely used in rodents and has permitted extensive studies of the regulation of the proliferation of these cells (for a review see Reference 23), using the “suicide” technique with tritiated thymidine.24 It has been established that the proliferation of CFU-S cells, quiescent in normal healthy mice, is controlled by stimulators25,26 and inhibitors.27-29 The latter have been identified as small peptides,30,31 which have been isolated from normal tissues. It is not yet known whether these physiological inhibitors could also be produced by malignant cells. Attempts to identify the stimulators have so far been unsuccessful. One might ask the question whether these activities could be, at least partly, related to the presence of IL-3 which was shown to stimulate CFU-S into the cell cycle both in vitro32 and in vivo.33
Effects of Hyperthermia On Hematopoietic Tissues
Published in Leopold J. Anghileri, Jacques Robert, Hyperthermia in Cancer Treatment, 2019
The only comprehensive study of the effects of heat on colony-forming cells of the three main lines of hematopoietic differentiation, to my knowledge, is the one we recently published.23In that study we examined in detail the time-temperature relationships of in vitro heating on mouse bone marrow cells. Figure 2 graphically represents clonogenic cell survival for each of the four progenitor populations exposed to 37, 42, 43, and 44°C. We studied CFU-GM, the granulocyte-macrophage precursor; CFU-M, the megakaryocyte colony-forming cell; and two erythroid progenitors, BFU-E and CFU-E. All of the survival curves are characterized by two main features: a shoulder region that is larger at 42°C, and smaller or not discernible at 44°C, followed by a phase in which cell survival declined exponentially with increasing time of exposure. In control incubations at 37°C, three of the four colonyforming populations were unaffected by culturing them for up to 3 hr: the frequency of colonies did not change. The lone exception, the CFU-E population declined slightly, but significantly, after 3 hr. We attributed this to the fact that maintenance of the CFU-E population is known to be dependent on erythropoietin. We carried out our incubations in the absence of exogenous hormone, a condition under which CFU-E numbers have been shown to decline within the time-frame of our studies.21
Genetic Control of Macrophage Antitumor Responses
Published in Gloria H. Heppner, Amy M. Fulton, Macrophages and Cancer, 2019
Mary M. Stevenson, Emil Skamene
The relationship between genetic variation of the proliferative potential of mononuclear phagocyte precursors and host response to neoplasia is presently undefined. However, variation among inbred strains of mice in macrophage proliferation has been described and genetic regulation is apparent at each of several, distinct developmental stages. Genetic regulation of the kinetics of proliferation of the multipotential stem cell has been well described.1-3 The earliest step of myelo-monocytopoiesis, namely in vitro granulocyte-macrophage colony-forming cell (CFC-GM) formation, has been found to vary quantitatively among inbred mouse strains, with the C57BL-derived strains exhibiting high bone marrow responsiveness to colony-stimulating factor (CSF).4,5 Such interstrain differences could be due to an augmented CSF-responsive bone marrow pool, to an intrinsic enhancement of the precursor cell’s responsiveness to CSF, to the magnitude of CFC-GM differentiation, or even possibly to the presence of CFC-GM inhibitors in the autologous sera used in the in vitro assay. The observation that the longevity of myelopoiesis in vitro (i.e., duration of generation of CFC-GM formation) varies markedly among strains of mice suggests that genetic regulation of CFC-GM formation is expressed as an intrinsic property of the precursor cell itself.6
Using miniature brain implants in rodents for novel drug discovery
Published in Expert Opinion on Drug Discovery, 2019
Therefore, the question arises how perfusion of human vasculature can be achieved in vivo. VEGF alone has been shown not to be sufficient to achieve perfusion in our experiments. Therefore, different strategies need to be chosen to perfuse the organoid with murine blood. It helps to look at results from other groups working on other organ systems to find a possible answer. The problem may be that VEGF alone does not lead to proliferation or ingrowth of mural vascular cells such as pericytes or α-smooth muscle cells. Alajati et al. showed that VEGF alone is not sufficient to perfuse a subcutaneous model of human endothelial cells [56]. However, when the group supplemented with PDGF-BB, human umbilical artery stem cells or human dermal fibroblasts, they were able to achieve approximately 20–35% perfusion of their xenograft in immunosuppressed mice [56]. Kang et al. [57] showed that human endothelial colony forming cell/mesenchymal progenitor cell-derived mesenchymal vessels could be perfused in a mouse model, even when re-implanted into a new mouse. Therefore, the presence of vascular mural cells besides endothelial cells seems to be mandatory for perfusion of the vasculature, which may also hold true for our human brain organoids.
Effect of hyperthermia on improving neutrophil restoration after intraperitoneal chemotherapy
Published in International Journal of Hyperthermia, 2019
Wan-Chun Huang, Chao-Chih Wu, Yun-Ting Hsu, Chih-Long Chang
Bone marrow suppression, another adverse effect of chemotherapy, affects the hematopoietic function of patients. To investigate whether hyperthermia could relieve this side effect, the mouse bone marrow cells were collected at different timepoints after treatment. The proliferation and differentiation patterns of bone marrow progenitor cells were analyzed using colony-forming cell assay. Although hyperthermia and control groups demonstrated no differences, the number of bone marrow cell CFUs were higher in the HIPEC group than in the IP chemotherapy group on Days 5, 10, and 15 after treatment (p < .05; Figure 4). The HSC and progenitor cell counts were then determined through flow cytometry (Figure 5(A)). HSC count in the bone marrow was higher in the HIPEC group than in the IP chemotherapy group (p < .05), particularly during the initial days (e.g., Day 5). Similarly, there were more pre-GMPs and GMPs in the HIPEC group than in the IP chemotherapy group (p < .05), particularly in later days (e.g., Day 15; Figure 5(B)). In general, the numbers of progenitor cells in the bone marrow were higher in mice that received HIPEC than in those that received IP chemotherapy.
The combined effects of hierarchical scaffolds and mechanical stimuli on ex vivo expansion of haematopoietic stem/progenitor cells
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Ji Eun Kim, Eun Jin Lee, Yanru Wu, Yun Gyeong Kang, Jung-Woog Shin
Hematopoietic potency was evaluated using the colony-forming cell (CFC) assay. On day 7, HSPCs were suspended in a semi-solid methylcellulose medium (MethoCult GF H4434; StemCell Technologies) and plated (in triplicate) in 35-mm-diameter Petri dishes at 1 × 103 cells/dish, followed by incubation in a conventional incubator (under 5% [v/v] CO2 at 37 °C) for 14 days. CFCs were counted on day 14, and morphologically distinguished: burst-forming unit-erythroids (BFU-E), colony-forming unit-granulocytes/macrophages (CFU-GM), and colony-forming unit-granulocytes/erythroids/macrophages/megakaryocytes (CFU-GEMM).