U-937 cells

U-937 cell <4> (<4> high expression of j6-ARK 1 [10]) [10] brain <1, 3, 6, 8> (<3> cerebral cortex [2-9] <3> highest -ARK activity in cerebral cortex [3] <3> highest j6-ARK mRNA concentrations in brain and spleen, brain highest levels in cerebral cortex and cerebellum, with significant lower levels in basal ganglia, brain stem, pituitary and hypothalamus [6] <6,8> regional and cellular distribution of -ARK 1 and 2 in brain [21]) [1-9, 11, 12, 21]... 

Yao Y, Sei Y, Abbracchio MP, Jiang JL, Kim YC, Jacobson KA (1997) Adenosine A3 receptor agonists protect HL-60 and U-937 cells from apoptosis induced by A3 antagonists. Biochem Biophys Res Commun 232(2) 317-322... 

Winkler JD, Sarau HM, Foley JJ et al. (1988) Leukotriene B4-induced homologous desensitization of calcium mobilization and phosphoinositide metabolism in U-937 cells. J Pharmacol Exp Ther 246 204-210... 

The mechanism by which Cell-Tak protein accomplishes this efficiency at the molecular level is addressed with the observation that different cell types attach with the same kinetics (Figure 2A). The lymphoma line (U-937), BHK cells, and bovine corneal endothelial cells attach with varying efficiencies to plastic (Figure 2B) but exhibit the same rate and overall efficiency on Cell-Tak protein. The attachment lacks the specificity that would indicate receptor-mediated attachment and supports the roll of nonspecific interactions. Moreover, other data (not shown) suggest that the attachment of cells is due to Cell-Tak and not to any component such as fibronectin that is found in serum. This is seen in experiments involving the preincubation of Cell-Tak-coated dishes with either fibronectin or serum. Cell-Tak-coated plates were preincubated with cell culture medium containing 20% calf serum for 30 min, and fibronectin was dried onto other plates coated with Cell-Tak before U-937 cells were plated. Cell attachment on fibronectin-coated Cell-Tak plates was identical to attachment to Cell-Tak alone, and attachment efficiency was inhibited by 40% on plates preincubated with serum. 

Figure 1. The attachment of adherent BHK-21 cells (Figure 1A) and nonadherent U-937 cells (Figure IB) to Cell-Tak adhesive, collagen, O poly-D-lysine, + laminin, X fibronectin, A and plastic, y, was monitored by counting unattached cells at 5, 12.5, and 20 min. Data were then converted mathematically to percent attached of those seeded.

Figure 2. The attachment kinetics of adherent BCE cells, O BHK-21 cells, + and nonadherent U-937 cells, , were compared directly on Cell-Tak adhesive (Figure 2A) and uncoated tissue culture plasticware (Figure 2B).

The growth rate of BCE cells is not altered in the presence of Cell-Tak protein (Figure 6). The same data have been obtained with other adherent types (BHK-21, data not shown). After attachment, nonadherent cells do not grow as discrete colonies, precluding the same type of evaluation with U-937 cells. 

Sane, A.T. and R. Bertrand, Caspase inhibition in camptothecin-treated U-937 cells is coupled with a shift from apoptosis to transient G1 arrest followed by necrotic cell death. Cancer Res, 1999. 59(15) p. 3565-9. 

Obermajer N, et al. Carboxypeptidase cathepsin X mediates beta2-integrin-dependent adhesion of differentiated U-937 cells. Exp. Cell Res. 2006 312 2515-2527. 

Trabelsi, N., Greffard, A., Pairon, J., Bignon, J., Zanetti, G., Fubini, B. and Pilatte, Y. (1997) Alterations in protein glycosylation in PMA-differentiated U-937 cells exposed to mineral particles. Environmental Health Perspectives, 105 (Suppl. 5), 1153-1158. 

Iwamoto, S., Takeda, K., Kamijo, R., and Konno, K., Induction of resistance to TNF cytotoxicity and mitochondrial superoxide dismutase on U-937 cells by 1,25-dihydroxyvitamin D3. Biochem. Biophys. Res. Common. 170, 73-79 (1990). 

Pan MH, Liang YC, Lin-Shiau SY, Zhu NQ, Ho CT, Lin JK. Induction of apoptosis by the oolong tea polyphenol theasinensin A through cytochrome c release and activation of caspase-9 and caspase-3 in human U-937 cells. J Agri Food Chem 2000 48 6337-6346. 

Maintenance of a cisoid restricted conformation about bonds C-6—C-7 and C-12—C-13 (structures types II and III) can provide activity equal to or better than that exhibited by all-rra/w-retinoic acid in most assays. TTNPB (3), TTNN (4), and (R12) (see Table 1.1) are marked by these restrictions and are parents to other type-II retinoids. In the induction of terminal differentiation of HL-60 and U-937 cells, however, removal of the latter conformational restriction results in enhanced activity. The tetramethyl-tetrahydronaphthyl-octatrienoic retinoid (structure type I, X=CMc2, aromatic ring B) is more potent than TTNPB, especially when either retinoid is administered in combination with cytokines (see POTENTIATIVE AND SYNERGISTIC EFFECTS USING RETINOIDS IN COMBINATION WITH CYTOKINES AND OTHER HORMONES below). 

The first total synthesis of dykellic acid (568) from (565-567), its derivatives, and the biological evaluation of these compounds have been achieved by Hergenrother and co-workers (Scheme 138). The results showed that dykellic acid strongly protected U-937 cells from apoptosis as induced by two distinct proapoptotic stimuli, etoposide and rotenone. 

Boles etal. (2000) demonstrated that 12-0-tetradecanoylphorbol-13-acetate enhanced the adherence of U-937 cells to fibronectin matrices by increasing the expression of both the a - and Pr subunit mRNAs and the surface expression of the protein. Modulation of OsPi expression may be important for regulation of monocytic cell function in lung inflammation after injury. 

Expression of tissue thromboplastin and urokinase-type plasminogen activator (EC 3.4.21.73) receptor were stimulated in monocyte-like U-937 cells treated with 5 ng 12-0-tetradecanoylphorbol-13-acetate per ml (Haase et al. 1993). 

Bryostatin 1 increased the susceptibility of U-937 cells to taxol-induced apoptosis and inhibition of clonogenicity (Wang et al. 1998). Bryostatin induced multiubiquitinylation of protein kinase C-a in vitro and in renal epithelial cells (Lee et al. 1996). In vitro multiubiquitinylation required ATP (or ATP6S), membranes containing the 76-kDa, nonphosphorylated form of protein kinase C, and a cytsol fraction (Lee et al. 1996). In primary cultures of human dermal fibroblasts bryostatin 1 and phorbol myristate acetate down-modulated protein kinase C-a and -e via the ubiquitin/proteasome pathway (Lee et al. 1997). 

Dehydroascorbic acid, the two-electron oxidised form of the vitamin, is taken up on the glucose transporter and reduced to ascorbate to a much greater extent than ascorbate itself is accumulated in human monocytic U-937 cells (May et al. 1999). In contrast to de droascorbic acid, ascorbate enters the cells in a sodium- and energy-dependent transporter. 

U-937 cells, a myelomonocytic cell line derived from a patient with histiocytic lymphoma, when differentiated by phorbol myristate acetate and exposed to DQ12 quartz (specific area 3 mVg), Mn02... 

Totpal K, Chaturvedi MM, LaPushin R, Aggarwal BB (1995) Retinoids downregulate both p60 and p80 forms of tumor necrosis factor receptors in human histiocytic lymphoma U-937 cells. Blood 85 3547-3555... 

---