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Transient Erythroblastopenia of Childhood
Published in Stephen A. Feig, Melvin H. Freedman, Clinical Disorders and Experimental Models of Erythropoietic Failure, 2019
Koenig and co-workers initially reported that normal erythroid colony formation in vitro was inhibited by fractionated immunoglobulin G (IgG) and/or serum from patients with TEC.27 This suppressive effect on colony growth disappeared as TEC improved. Moreover, these authors demonstrated that erythroid colony growth from marrow of a patient with TEC did not grow in the presence of autologous serum but did form colony-forming units-erythroid (CFU-E) and burst-forming units-erythroid (BFU-E) in the presence of normal serum. In these studies erythroid colony formation from CFU-E was suppressed more than the more primitive BFU-E. Thus, because BFU-E have a higher erythropoietin (EPO) requirement than CFU-E, Koenig et al.27 speculated that the inhibitory effect is due to immune suppression of erythroid progenitor cells and not due to direct inhibition of EPO.
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
Quantitative Assays for Human Hemopoietic Progenitor Cells
Published in Adrian P. Gee, BONE MARROW PROCESSING and PURGING, 2020
Heather J. Sutherland, Allen C. Eaves, Connie J. Eaves
For each of the myeloid pathways it is possible to obtain colonies resulting from the proliferation of a progenitor committed to that differentiation lineage. Erythropoietic progenitors generate colonies that, at the end of their growth phase, are made up of clusters of hemoglobinized erythroblasts. The number of such clusters in each colony provides a rough estimate of the size of the mature colony, and hence can be used to subdivide clonogenic erythropoietic progenitors according to their varying proliferative capacities. The most mature erythroid progenitors are referred to as colony-forming-unit-erythroid (CFU-E), the more primitive as burst-forming-unit-erythroid (BFU-E). In man, CFU-E are defined as progenitors that produce only one or two clusters containing from 8 to ~100 hemoglobinized erythroblasts, and maturation of the cells within such colonies is usually complete by 10 to 12 days after initiation of the culture. Thereafter, these small erythroid colonies become more difficult to identify, as the cells within them begin to lyse and CFU-E-derived colony counts thus appear to decline.6 BFU-E may be readily subdivided into those that produce small (3 to 8 clusters), intermediate (9 to 16 clusters), or large (more than 16 clusters) colonies. The division between erythroid colonies produced by mature and primitive BFU-E subpopulations has technical as well as biological relevance. The smaller colonies reach maturity sooner and are best counted at approximately the same time as those derived from CFU-E, whereas those that achieve a larger size also mature later and are therefore not optimally evaluated until 18 to 20 days in culture have elapsed. Additionally, mature BFU-E, like CFU-E, represent a more rapidly turning over population in normal marrow than primitive BFU-E and are physically larger cells.8,36
Responses of hematopoietic cells after ionizing-irradiation in anemic adult medaka (Oryzias latipes)
Published in International Journal of Radiation Biology, 2023
Kento Nagata, Keita Ohashi, Chika Hashimoto, Alaa El-Din Hamid Sayed, Takako Yasuda, Bibek Dutta, Takayuki Kajihara, Hiroshi Mitani, Michiyo Suzuki, Tomoo Funayama, Shoji Oda, Tomomi Watanabe-Asaka
In adult mammals, hematopoietic tissue is located in the bone marrow and blood cells such as erythrocytes, platelets and leucocytes originate from the respective hematopoietic stem cells (HSC). Progenitor cells are produced from HSCs and can only differentiate into the respective blood cell types. Among the cells that differentiate into erythrocytes, polychromatic erythroblasts and those at the earlier differentiation stages are proliferative (Orkin 2000; Doing 2007). HSCs and hematopoietic progenitor cells are particularly radiosensitive (Imai and Nakao 1987; Ploemacher et al. 1992; Wang et al. 2006; Heylmann et al. 2014; Guo et al. 2015) and exposure to lethal doses of IR causes death of HSCs, leading to irreversible anemia, immune deficiency, and death of the individual. In the case of sub-lethal dose of IR, HSCs arrest their cell cycle and repair DNA damages, while proliferating erythroid progenitor cells (BFU-E and CFU-E) undergo apoptosis and die. Several days after the irradiation, HSCs repair the DNA damages and resume hematopoiesis (Shao et al. 2014). In contrast, differentiated cells further than polychromatic erythroblasts, which have lost their mitotic potential, do not undergo apoptosis (Peslak et al. 2011). Mature mammalian erythrocytes are enucleated and highly radio-resistant, but the density of erythrocytes in the peripheral blood decreases temporarily due to exposure-induced damages of the erythrocytes (Gwoździński 1991; Puchała et al. 2004), and the cell density recovers when hematopoiesis resumes (Okunewick and Phillips 1972; Peslak et al. 2011).
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
For all three cell populations analyzed (HSCs, MPCs, and EPCs), purity was >98% (Supplemental Figure 1A). In terms of CFC content, 18 ± 5% of HSCs were capable of forming hematopoietic colonies in semisolid cultures. Among such CFCs, 4% of them gave rise to colonies containing both myeloid and erythroid cells, 49% gave rise to myeloid colonies, including both granulocytic and monocitic colonies, and 47% gave rise to erythroid colonies (Supplemental Figure 1B). The majority of the latter consisted of large erythroid colonies (BFU-E). In the MPC population, 9 ± 5% of the cells were CFCs; 95% of them gave rise to myeloid colonies and 5% to small erythroid colonies (CFU-E). Finally, 24 ± 6% of the cells in the EPC population were CFCs; 97% of them gave rise to both large and small erythroid colonies, and 3% to small myeloid colonies. No myeloid-erythroid colonies were observed in the MPC or EPC populations (Supplemental Figure 1B).
Autophagy-deficiency in bone marrow mononuclear cells from patients with myasthenia gravis: a possible mechanism of pathogenesis
Published in International Journal of Neuroscience, 2021
Jingqun Tang, Ziming Ye, Yi Liu, Mengxiao Zhou, Liqiang Huang, Qin Mo, Xiaotao Su, Chao Qin
The colony-forming potential of BM-MNCs is shown in Figure 2a. The mean (± SD) number of CFU-GM obtained by 105 BM-MNCs was significantly lower in BMG patients than in the controls (39.84 ± 6.26 vs. 58.50 ± 7.54, respectively, p < 0.05), while the frequency (mean ± SD) of CFU-Meg in BMG patients was higher than that in the controls (79.53 ± 10.62 vs. 41.17 ± 6.94, respectively, p < 0.05). However, the mean number of CFU-E did not show a significant difference between the BMG patients and the normal controls (94.53 ± 11.77 vs. 98.25 ± 13.35, respectively, p > 0.05). Interestingly, the amount of CFU-Meg colony formation (mean ± SD) in GMG was significantly higher than that in OMG (87.31 ± 9.36 vs. 71.17 ± 6.62, p < 0.05, respectively), whereas the frequency (mean ± SD) of CFU-GM in GMG was lower than that in OMG (37.38 ± 5.78 vs.45.17 ± 3.31, p < 0.05, respectively) (Figure 2b).