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Cell Adhesion in Animal Cell Culture: Physiological and Fluid-Mechanical Implications
Published in Martin A. Hjortso, Joseph W. Roos, Cell Adhesion, 2018
Manfred R. Koller, Eleftherios T. Papoutsakis
The staggering number of mature cells that must be continuously produced under normal unstressed conditions are derived from progenitor (or precursor) cells. These progenitor cells are unipotential or bipotential and are therefore capable of undergoing proliferation, differentiation, and development into only one or two of the mature cell types. These progenitor cells are designated by the term “colony-forming unit,” CFU (or “colony-forming cell,” CFC), because of their ability to form colonies of mature cells in semisolid agar culture. To specify the type of progenitor, a suffix is simply added to the CFU-designation. For example, granulocyte/macrophage colony-forming units (CFU-GM) proliferate and develop into mature neutrophils and macrophages. Erythroid colony-forming units (CFU-E) undergo growth and hemoglobinization to form mature erythrocytes. Similarly, other lineage-restricted progenitor cells have been described that give rise to eosinophils (CFU-Eos), basophils (CFU-Bas), and megakaryocytes (CFU-Meg) (133). In adult animals, these myeloid progenitor cells are located mainly in the bone marrow, with small populations in the spleen and the circulation. It therefore follows that the bone marrow is the major site of myeloid blood cell production in adults. B-cell progenitors are found in the bone marrow, spleen, and lymphoid tissues, while T-cell progenitors are formed only in the thymus and from there may migrate to other lymphoid tissues. Like the mature cells they produce, most progenitor cells are short-lived because as they proliferate, they concomitantly undergo development and lose their proliferative potential.
The potential interaction of environmental pollutants and circadian rhythm regulations that may cause leukemia
Published in Critical Reviews in Environmental Science and Technology, 2022
Francisco Alejandro Lagunas-Rangel, Błażej Kudłak, Wen Liu, Michael J. Williams, Helgi B. Schiöth
Phthalates are commonly used in medical devices and in personal care products such as soaps, lubricating oils, hairsprays, perfumes, cosmetics, and shampoos. The L5178Y mouse lymphoma mammalian cell mutation assay demonstrated mutagenic activity of dimethyl phthalate (DMP) and DBP, but only in the presence of hepatic S9 pools that are a rich source of drug metabolizing enzymes, including those of the P-450 family, suggesting that the damage is caused primarily by its metabolites. This was not the case for butyl benzyl phthalate (BBP), di-{n hexyl, n-octyl, n-decyl} phthalate (610 P), di-isononyl phthalate (DINP), di-{heptyl, nonyl, undecyl} phthalate (711 P), diisodecyl phthalate (DIDP) and di-undecyl phthalate (DUP) (Barber et al., 2000). On the other hand, exposure to DBP at a concentration of 100 μg/mL for four days was shown to selectively affect the viability of acute myeloid leukemic blast progenitor cells (AML-CFU), but not of normal granulocyte/macrophage progenitor cells (CFU-GM) (Wu et al., 1995). Apoptosis was also caused in acute megakaryoblastic leukemia cells M-O7e and histiocytic lymphoma U-937 using DBP at a concentration of 100 μg/mL, as well as in cells of promyelocytic leukemia HL-60 with a concentration of 50 μg/mL for nine days (Chu-Tse et al., 1993; L.-S. Wang et al., 2002). In a clinical trial in patients with AML, bone marrow samples were collected for autotransplantation. For this, bone marrow collection bags containing a culture medium with DBP were used and after 6 days the medium was replaced with medium without DBP. In this manner, a significant reduction in the number of leukemic cells was observed, but an adequate number of normal cells was maintained to repopulate the bone marrow of the patients. Thus, DBP was considered as a purging agent (Lisheng et al., 1996). Meanwhile, di(2-ethylhexyl) phthalate (DEHP) was shown to cause apoptosis in HL-60 promyelocytic leukemia cells, mainly at high doses (over 100 μg/mL), and also reduce cell migration at low doses (10 μg/mL). Its metabolite, MEHP, required lower doses to cause apoptosis (50 μg/mL), but higher doses to affect cell migration (25 μg/mL) (Manz et al., 2014). Regarding the circadian clock genes, it was shown that DEHP significantly alters their levels, increasing the expression of CLOCK, CRY1 and NR1D1, but decreasing the expression of PER2 and PER3 (Table 1) (Currie et al., 2005).