Establishment and characterization of a human histiocytic lymphoma cell line (U‐937)

Sundström, Christer; Nilsson, Kenneth

doi:10.1002/ijc.2910170504

Cited by 2,234 publications

(967 citation statements)

References 57 publications

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“…The human monocytic cell line U937 was obtained from American Type Culture Collection (ATCC; Rockville, MD). The U937 cell line expresses the HLA class I alleles A3, A26, B18, B51, Cw1, and Cw3 (22). U937 cells were cotransfected with HLA-B*2705 genomic DNA (B27g) (23), mutated HLA-B*2705 genomic DNA (see below), or HLA-A2 genomic DNA (24) and pSV2neo (to confer resistance to Geneticin [G-418]) by electroporation as described previously (4).…”

Section: Methodsmentioning

confidence: 99%

Enhanced intracellular replication of Salmonella enteritidis in HLA–B27–expressing human monocytic cells: Dependency on glutamic acid at position 45 in the B pocket of HLA–B27

Penttinen¹,

Heiskanen²,

Mohapatra³

et al. 2004

Arthritis & Rheumatism

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Objective. To reveal the cause of the impaired elimination of Salmonella enteritidis in HLA-B27-transfected human monocytic cells and to study whether the B pocket of HLA-B27 contributes to these modulatory effects.Methods. Stable U937 cell transfectants expressing HLA-A2, B27, or different forms of B27 with amino acid substitutions in the B pocket were prepared. Mocktransfected cells were prepared using the antibiotic resistance vector (pSV2neo) alone. Cells were differentiated, infected with S enteritidis, and the number of live intracellular S enteritidis organisms was determined using the colony-forming unit method. To visualize intracellular S enteritidis, the bacteria were transformed with green fluorescent protein (GFP), and studied by confocal microscopy.Results. Cells expressing wild-type HLA-B27 were more permissive of intracellular replication of S enteritidis compared with mock-transfected or A2-transfected controls. Cells expressing B27 with an altered B pocket composition having either 6 amino acid substitutions (B27.A2B; substitutions H9F, T24A, E45M, I66K, C67V, and K70H) or a single substitution (B27.E45M) were no longer permissive of S enteritidis replication. In contrast, cells expressing B27 with the single substitution of F for H at position 9 (B27.H9F) retained their permissiveness. Studies using GFPtransformed S enteritidis confirmed that the increase in the amount of intracellular bacteria in B27-expressing cells was due to replication of the bacteria.Conclusion. Our data indicate that HLA-B27 expression modulates the host-microbe interaction that results in an impaired capacity of monocytes to resist intracellular replication of S enteritidis. The phenotype is dependent on glutamic acid at position 45 in the B pocket and, thus, may be due to properties of the B27 heavy chain that are related to this residue. The ability of HLA-B27 to confer susceptibility to Salmonellatriggered reactive arthritis may occur, at least in part, through these modulatory effects.

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Section: Methodsmentioning

confidence: 99%

Enhanced intracellular replication of Salmonella enteritidis in HLA–B27–expressing human monocytic cells: Dependency on glutamic acid at position 45 in the B pocket of HLA–B27

Penttinen¹,

Heiskanen²,

Mohapatra³

et al. 2004

Arthritis & Rheumatism

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“…The human monocytic cell line U937 was obtained from the American Type Culture Collection (ATCC CRL-1593.2) (13). Cells were maintained in Iscove's modified Dulbecco's medium (IMDM) supplemented with 10% fetal calf serum, 100 units/ml penicillin, and 50μg/ml streptomycin at 37 C, 5% CO 2 .…”

Section: Cellsmentioning

confidence: 99%

Oxidized LDL immune complexes and oxidized LDL differentially affect the expression of genes involved with inflammation and survival in human U937 monocytic cells

et al. 2009

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Objective-To compare the global effects of oxidized LDL (oxLDL) and oxLDL-containing immune complexes (oxLDL-IC) on gene expression in human monocytic cells and to identify differentially expressed genes involved with inflammation and survival.Methods and Results-U937 cells were treated with oxLDL-IC, oxLDL, Keyhole limpet hemocyanin immune complexes (KLH-IC), or vehicle for 4 h. Transcriptome profiling was performed using DNA microarrays. oxLDL-IC uniquely affected the expression of genes involved with pro-survival (RAD54B, RUFY3, SNRPB2, and ZBTB24). oxLDL-IC also regulated many genes in a manner similar to KLH-IC. Functional categorization of these genes revealed that 39% are involved with stress responses, including the unfolded protein response which impacts cell survival, 19% with regulation of transcription, 10% with endocytosis and intracellular transport of protein and lipid, and 16% with inflammatory responses including regulation of I-κB/NF-κB cascade and cytokine activity. One gene in particular, HSP70 6, greatly up-regulated by ox-LDL-IC, was found to be required for the process by which oxLDL-IC augments IL1-β secretion. The study also revealed genes uniquely up-regulated by oxLDL including genes involved with growth inhibition (OKL38, NEK3, and FTH1), oxidoreductase activity (SPXN1 and HMOX1), and transport of amino acids and fatty acids (SLC7A11 and ADFP).Conclusions-These findings highlight early transcriptional responses elicited by oxLDL-IC that may underlie its cytoprotective and pro-inflammatory effects. Cross-linking of Fcγ receptors appears to be the trigger for most of the transcriptional responses to oxLDL-IC. The findings further strengthen the hypothesis that oxLDL and oxLDL-IC elicit disparate inflammatory responses and play distinct roles in the process of atherosclerosis.

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“…The U937 (Sundstrom and Nilsson, 1976) and HL-60 (Collins et al, 1977) cell lines were obtained from ATCC and maintained as described (Vrana et al, 1998). Transfectant U937 cells stably overexpressing Bcl-2 or Bcl-x L were generated by electroporation of the parental line with a plasmid (pCEP4 or pcDNA3.1; Invitrogen) containing Bcl-2 or Bcl-x L cDNA (Wang et al, 1997).…”

Section: Cell Linesmentioning

confidence: 99%

“…The myelomonocytic cell line U937 (Sundstrom and Nilsson, 1976) matures along a monocyte/macrophage lineage in response to tumorpromoting phorboids such as PMA (Hass et al, 1991). In the present study, the capacities of SAHA and HMBA to induce di erentiation and apoptosis in U937 cells have been compared in order to identify determinants of these fundamentally di erent cellular fates.…”

mentioning

confidence: 99%

Induction of apoptosis in U937 human leukemia cells by suberoylanilide hydroxamic acid (SAHA) proceeds through pathways that are regulated by Bcl-2/Bcl-XL, c-Jun, and p21CIP1, but independent of p53

et al. 1999

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Determinants of di erentiation and apoptosis in myelomonocytic leukemia cells (U937) exposed to the novel hybrid polar compound SAHA (suberoylanilide hydroxamic acid) have been examined. In contrast to hexamethylenbisacetamide (HMBA), SAHA-related maturation was limited and accompanied by marked cytoxicity. SAHA-mediated apoptosis occurred within the G 0 G 1 and S phase populations, and was associated with decreased mitochondrial membrane potential, caspase-3 activation, PARP degradation, hypophosphorylation/cleavage of pRB, and down-regulation of c-Myc, c-Myb, and B-Myb. Enforced expression of Bcl-2 or Bclx L inhibited SAHA-induced apoptosis, but only modestly potentiated di erentiation. While SAHA induced the cyclin-dependent kinase inhibitor p21 CIP1 , antisense ablation of this CDKI increased, rather than decreased, SAHA-related lethality. In contrast, conditional expression of wild-type p53 failed to modify SAHA actions, but markedly potentiated HMBA-induced apoptosis. Finally, SAHA modestly increased expression/activation of the stress-activated protein kinase (SAPK/JNK); moreover, SAHA-related lethality was partially attenuated by a dominant-negative c-Jun mutant protein (TAM67). SAHA did not stimulate mitogen-activated protein kinase (MAPK), nor was lethality diminished by the speci®c MEK/MAPK inhibitor PD98059. These ®ndings indicate that SAHA potently induces apoptosis in human leukemia cells via a pathway that is p53-independent but at least partially regulated by Bcl-2/Bcl-x L , p21 CIP1 , and the c-Jun/AP-1 signaling cascade.

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Establishment and characterization of a human histiocytic lymphoma cell line (U‐937)

Cited by 2,234 publications

References 57 publications

Enhanced intracellular replication of Salmonella enteritidis in HLA–B27–expressing human monocytic cells: Dependency on glutamic acid at position 45 in the B pocket of HLA–B27

Enhanced intracellular replication of Salmonella enteritidis in HLA–B27–expressing human monocytic cells: Dependency on glutamic acid at position 45 in the B pocket of HLA–B27

Oxidized LDL immune complexes and oxidized LDL differentially affect the expression of genes involved with inflammation and survival in human U937 monocytic cells

Induction of apoptosis in U937 human leukemia cells by suberoylanilide hydroxamic acid (SAHA) proceeds through pathways that are regulated by Bcl-2/Bcl-XL, c-Jun, and p21CIP1, but independent of p53

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