Increased sensitivity of a xeroderma pigmentosum lymphoblastoid cell line to serum deprivation in vitro

In Vitro ◽  
1983 ◽  
Vol 19 (8) ◽  
pp. 621-624 ◽  
Author(s):  
W. Clark Lambert ◽  
Muriel W. Lambert
Keyword(s):  
Cell Line ◽  
Xeroderma Pigmentosum ◽  
Lymphoblastoid Cell Line ◽  
Serum Deprivation ◽  
Increased Sensitivity

scholarly journals Opposite effects of recombinant interferon-alpha A and deoxycoformycin on adenosine deaminase activity in the Daudi B lymphoblastoid cell line

Blood ◽  
1988 ◽  
Vol 71 (1) ◽  
pp. 59-64 ◽  
Author(s):  
CR Faltynek
Keyword(s):  
Growth Inhibition ◽  
Cell Line ◽  
Adenosine Deaminase ◽  
Interferon Alpha ◽  
Lymphoblastoid Cell Line ◽  
Recombinant Interferon ◽  
Growth Inhibitory ◽  
Adenosine Deaminase Activity ◽  
Recombinant Interferon Alpha

Abstract Interferon-alpha and the adenosine deaminase (ADA) inhibitor deoxycoformycin (dCF) have each been shown to be efficacious in the treatment of some lymphoid malignancies and to have potent antiproliferative activities in vitro. This study examined whether dCF and recombinant interferon-alpha A (rIFN-alpha A) were additive, synergistic, or antagonistic in their effects on the cultured B lymphoblastoid cell line Daudi. Treatment of Daudi cells for three to four days with doses of rIFN-alpha A that were growth inhibitory was unexpectedly found to increase the level of ADA activity per cell two- to threefold and therefore to prevent the inhibition of ADA by limiting concentrations of dCF. However, the opposite effects of dCF and rIFN- alpha A on ADA activity did not lead to antagonistic effects on growth inhibition. The higher concentrations of dCF (with deoxyadenosine) necessary for appreciable growth inhibition could inhibit the increased ADA activity in rIFN-alpha A-treated cells, thus resulting in additive antiproliferative effects.

scholarly journals Combination of Tenofovir and Emtricitabine with Efavirenz Does Not Moderate Inhibitory Effect of Efavirenz on Mitochondrial Function and Cholesterol Biosynthesis in Human T Lymphoblastoid Cell Line

2018 ◽  
Vol 62 (9) ◽  
Author(s):  
Min Li ◽  
Anuoluwapo Sopeyin ◽  
Elijah Paintsil
Keyword(s):  
Cell Line ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Lymphoblastoid Cell Line ◽  
Cholesterol Biosynthesis ◽  
Real Life ◽  
Mitochondrial Toxicity ◽  
And Function

ABSTRACT Efavirenz (EFV), the most popular nonnucleoside reverse transcriptase inhibitor, has been associated with mitochondrial dysfunction in most in vitro studies. However, in real life the prevalence of EFV-induced mitochondrial toxicity is relatively low. We hypothesized that the agents given in combination with EFV moderate the effect of EFV on mitochondrial function. To test this hypothesis, we cultured a human T lymphoblastoid cell line (CEM cells) with EFV alone and in combination with emtricitabine (FTC) and tenofovir disoproxil fumarate (TDF) to investigate the effects on mitochondrial respiration and function and cholesterol biosynthesis. There was a statistically significant concentration- and time-dependent apoptosis, reduction in mitochondrial membrane potential, and increase in production of reactive oxygen species in cells treated with either EVF alone or in combination with TDF plus FTC. Compared to dimethyl sulfoxide-treated cells, EFV-treated cells had significant reduction in oxygen consumption rate contributed by basal mitochondrial respiration and decreased protein expression of electron transport chain complexes (CI, CII, and CIV). Treatment with EFV resulted in a decrease in mitochondrial DNA content and perturbation of more coding genes (n = 13); among these were 11 genes associated with lipid or cholesterol biosynthesis. Our findings support the growing body of knowledge on the effects of EFV on mitochondrial respiration and function and cholesterol biosynthesis. Interestingly, combining TDF and FTC with EFV did not alter the effects of EFV on mitochondrial respiration and function and cholesterol biosynthesis. The gap between the prevalence of EFV-induced mitochondrial toxicity in in vitro and in vivo studies could be due to individual differences in the pharmacokinetics of EFV.

scholarly journals Lymphoblastoid cell line with B1 cell characteristics established from a chronic lymphocytic leukemia clone by in vitro EBV infection

2012 ◽  
Vol 1 (1) ◽  
pp. 18-27 ◽  
Author(s):  
Anders Rosén ◽  
Ann-Charlotte Bergh ◽  
Peter Gogok ◽  
Chamilly Evaldsson ◽  
Anna Lanemo Myhrinder ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Cell Line ◽  
Lymphoblastoid Cell Line ◽  
Lymphocytic Leukemia ◽  
Ebv Infection

scholarly journals An Epstein-Barr Virus Isolated from a Lymphoblastoid Cell Line Has a 16-Kilobase-Pair Deletion Which Includes gp350 and the Epstein-Barr Virus Nuclear Antigen 3A

2001 ◽  
Vol 75 (18) ◽  
pp. 8556-8568 ◽  
Author(s):  
Wonkeun Lee ◽  
Yoon-Ha Hwang ◽  
Suk-Kyeong Lee ◽  
Chitra Subramanian ◽  
Erle S. Robertson
Keyword(s):  
Cell Line ◽  
B Lymphocytes ◽  
Epstein Barr Virus ◽  
Lymphoblastoid Cell Line ◽  
Phorbol Esters ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Amino Terminal ◽  
Epstein Barr

ABSTRACT Epstein-Barr virus (EBV) is associated with human cancers, including nasopharyngeal carcinoma, Burkitt's lymphoma, gastric carcinoma and, somewhat controversially, breast carcinoma. EBV infects and efficiently transforms human primary B lymphocytes in vitro. A number of EBV-encoded genes are critical for EBV-mediated transformation of human B lymphocytes. In this study we show that an EBV-infected lymphoblastoid cell line obtained from the spontaneous outgrowth of B cells from a leukemia patient contains a deletion, which involves a region of approximately 16 kbp. This deletion encodes major EBV genes involved in both infection and transformation of human primary B lymphocytes and includes the glycoprotein gp350, the entire open reading frame of EBNA3A, and the amino-terminal region of EBNA3B. A fusion protein created by this deletion, which lies between the BMRF1 early antigen and the EBNA3B latent antigen, is truncated immediately downstream of the junction 21 amino acids into the region of the EBNA3B sequence, which is out of frame with respect to the EBNA3B protein sequence, and indicates that EBNA3B is not expressed. The fusion is from EBV coordinate 80299 within the BMRF1 sequence to coordinate 90998 in the EBNA3B sequence. Additionally, we have shown that there is no detectable induction in viral replication observed when SNU-265 is treated with phorbol esters, and no transformants were detected when supernatant is used to infect primary B lymphocytes after 8 weeks in culture. Therefore, we have identified an EBV genome with a major deletion in critical genes involved in mediating EBV infection and the transformation of human primary B lymphocytes that is incompetent for replication of this naturally occurring EBV isolate.

scholarly journals Opposite effects of recombinant interferon-alpha A and deoxycoformycin on adenosine deaminase activity in the Daudi B lymphoblastoid cell line

Blood ◽  
1988 ◽  
Vol 71 (1) ◽  
pp. 59-64
Author(s):  
CR Faltynek
Keyword(s):  
Growth Inhibition ◽  
Cell Line ◽  
Adenosine Deaminase ◽  
Interferon Alpha ◽  
Lymphoblastoid Cell Line ◽  
Recombinant Interferon ◽  
Growth Inhibitory ◽  
Adenosine Deaminase Activity ◽  
Recombinant Interferon Alpha

Interferon-alpha and the adenosine deaminase (ADA) inhibitor deoxycoformycin (dCF) have each been shown to be efficacious in the treatment of some lymphoid malignancies and to have potent antiproliferative activities in vitro. This study examined whether dCF and recombinant interferon-alpha A (rIFN-alpha A) were additive, synergistic, or antagonistic in their effects on the cultured B lymphoblastoid cell line Daudi. Treatment of Daudi cells for three to four days with doses of rIFN-alpha A that were growth inhibitory was unexpectedly found to increase the level of ADA activity per cell two- to threefold and therefore to prevent the inhibition of ADA by limiting concentrations of dCF. However, the opposite effects of dCF and rIFN- alpha A on ADA activity did not lead to antagonistic effects on growth inhibition. The higher concentrations of dCF (with deoxyadenosine) necessary for appreciable growth inhibition could inhibit the increased ADA activity in rIFN-alpha A-treated cells, thus resulting in additive antiproliferative effects.

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