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At least 217 records · Page 12Linked to original sources
PubMed1995

Inhibition of apoptosis by antioxidants in the human HL-60 leukemia cell line.

Cell death via apoptosis is an important event involved in a number of immunological processes. Recently, apoptosis has been associated with oxidative stress in a number of cell systems. Here we assessed the inhibitory capacity of different antioxidants on UV- and drug-induced apoptosis in the human leukemic cell line, HL-60. We found that the oxygen radical scavenger, BHA, the radioprotector cysteamine and the metal chelators, pyrrolidinedithiocarbamate (PDTC), diethyldithiocarbamate (DEDTC), and dimethyldithiocarbamate (DMDTC), were able to significantly inhibit nuclear fragmentation and reduce the formation of apoptotic bodies in UV-irradiated human leukemic cells. Both BHA and PDTC were found to reduce DNA fragmentation as assessed by in situ DNA nick-end labelling and quantification thereof using fluorescence flow cytometry. In addition to inhibiting UV-induced apoptosis, PDTC was also capable of reducing the amount of apoptosis induced by a range of cytotoxic drugs, such as actinomycin-D, camptothecin, etoposide, and melphalan, whereas BHA and cysteamine were not as effective in these cases after more than four hours in culture when compared to PDTC. To further elucidate the working mechanism of PDTC, we have looked at the effect of PDTC on DNA fragmentation in isolated nuclei, under conditions that promote activation of endogenous endonuclease involved in apoptosis. In contrast to ZnCl2, a potent inhibitor of endonuclease activity, PDTC was unable to inhibit DNA-ladder formation in this assay. Taken together, these results indicate that oxygen radicals may have a central role to play in the induction of apoptosis and that dithiocarbamates can serve as potent inhibitors of apoptosis induced by a wide variety of stimuli.

Antioxidants↗
PubMed1995

Characterization of cis-regulatory elements of the c-myc promoter responding to human GM-CSF or mouse interleukin 3 in mouse proB cell line BA/F3 cells expressing the human GM-CSF receptor.

Interleukin 3 (IL-3) or granulocyte macrophage colony-stimulating factor (GM-CSF) activates c-fos, c-jun, and c-myc genes and proliferation in both hematopoietic and nonhematopoietic cells. Using a series of deletion mutants of the beta subunit of human GM-CSF receptor (hGMR) and inhibitors of tyrosine kinase, two distinct signaling pathways, one for activation of c-fos and c-jun genes, and the other for cell proliferation and activation of c-myc gene have been elucidated. In contrast to wealth of information on the pathway leading to activation of c-fos/c-jun genes, knowledge of the latter is scanty. To clarify the mechanisms of activation of c-myc gene by cytokines, we established a transient transfection assay in mouse proB cell line BA/F3 cells expressing hGMR. Analyses of hGMR beta subunit mutants revealed two cytoplasmic regions involved in activation of the c-myc promoter, one is essential and the other is dispensable but enhances the activity. These regions are located at the membrane proximal and the distal regions covering amino acid positions 455-544 and 544-589, respectively. Characterization of cis-acting regulatory elements of the c-myc gene showed that the region containing the P2 promoter initiation site is sufficient to mediate the response to mIL-3 or hGM-CSF. Electrophoretic mobility shift assay using an oligonucleotide corresponding to the distal putative E2F binding site revealed that p107/E2F complex, the negative regulator of E2F, decreased, and free E2F increased after mIL-3 stimulation. These results support the thesis that mIL-3 or hGM-CSF regulates the c-myc promoter by altering composition of the E2F complexes at E2F binding site.

Animals↗
PubMed1990

[In vitro prompt killing by chlorhexidine of human colorectal carcinoma cell lines].

Cell lines of human colorectal carcinoma were used to test the prompt killing effect of chlorhexidine in several concentrations of normal saline or distilled water 0.25g/L 5-fluorouracil in normal saline was used as positive control. Normal saline was used as negative control. It was found that chlorhexidine were more effective than 5-fluorouracil as shown by the proliferation of cells, the mitotic index and the morphology of cells. New passages of cells failed to proliferate and died in 19 days after chlorhexidine treatment. The authors came to the conclusion that 0.2g/L chlorhexidine in distilled water can be used for irrigation of the peritoneal and pelvic cavities on the end of colorectal carcinoma resection to prevent implantation metastasis and infection.

Adenocarcinoma↗
PubMed1995

1,25-Dihydroxyvitamin D3 suppresses cell growth, DNA synthesis, and phosphorylation of retinoblastoma protein in a breast cancer cell line.

Cells of a breast adenocarcinoma cell line, CAMA-IEe, were found to contain a moderate concentration of 1,25-dihydroxyvitamin D3[1,25(OH)2D3] receptors. The receptors' dissociation constant calculated by Scatchard analysis was 4.1 x 10(-10) M. These receptors sedimented at around 4.0 S position on a linear 5-20% sucrose density gradient and exhibited an apparent molecular weight of about 46 kDa. Receptor concentration was found to be highest in the early stages of cell growth, decreased continuously when cells were actively growing, and reached the lowest level at confluence. Suppression of cell growth, of DNA synthesis, and of the phosphorylation of retinoblastoma protein by 1,25(OH)2D3 at concentrations about 10(-7) M were observed. Treatment with 10(-7) M 1,25(OH)2D3 for 12 hr or longer caused elevation of cytosolic free calcium in CAMA-IEe cells. These results show that CAMA-IEe cell growth is suppressed by 1,25(OH)2D3 and that the suppression is possibly mediated through calcium mobilization.

Adenocarcinoma↗
PubMed1998

Chimeric CD4/CD44 molecules associate with CD44 via the transmembrane region and reduce hyaluronan binding in T cell lines.

Cells of the immune system tightly regulate the binding ability of cell adhesion molecules. The binding of the extracellular matrix component hyaluronan to CD44 is no exception, yet the mechanisms that regulate its binding are poorly understood. In this study a chimeric CD4/CD44 molecule, containing the extracellular domain of CD4 and the transmembrane and cytoplasmic domains of CD44, was expressed in two CD44+ mouse T lymphoma cell lines, BW5147 and T28. This resulted in the reduced ability of endogenous CD44 to constitutively bind hyaluronan. Immunoprecipitation of the chimeric protein in 1 % Brij-96 indicated an association between the chimera and endogenous CD44. Using various chimeric CD4/CD44 molecules, the transmembrane region of CD44 was found to mediate this association. In addition, the association of chimeric CD4/CD44 molecules with endogenous CD44 correlated with reduced hyaluronan binding. Thus, the transmembrane region of CD44 is required for the association with CD44 molecules in the cell membrane and we propose that the self-association of CD44 molecules occurs on the T cell surface to promote hyaluronan binding. Cellular events altering the interactions of the transmembrane region of CD44 thus have the potential to regulate the hyaluronan binding ability of CD44.

3T3 Cells↗
PubMed2001

Characteristics of etoposide-induced apoptotic cell death in the U-937 human lymphoma cell line.

Cell death induced by etoposide in the human lymphoma cell line U-937 GTB was characterized. Activity of caspases -3, -8 and -9 was measured by spectrophotometric detection of specific cleavage products, DNA fragmentation by TdT-mediated dUTP nick end-labelling (TUNEL), and apoptotic morphology by conventional staining and microscopy, as well as by a novel method-the microculture kinetics (MiCK) assay. Synthesis of protein and DNA during exposure was monitored by incorporation of radioactive leucine and thymidine, respectively. The effects of caspase inhibitors on total viability, as well as early and late morphological changes were studied. Etoposide rapidly induced apoptosis, dependent on caspase-3 and -8, but inhibition of these caspases did not prevent major cell death, but promoted a switch in late morphology. The novel MiCK assay added valuable information on early morphological events during cell death. Hence, this study provides support for caspase-8-mediated apoptosis in U-937 GTB when exposed to etoposide. General caspase inhibition switches cell death to one with a different morphology.

Apoptosis↗
PubMed1982

Cell cycle analysis in a human cell line (EUE cells).

A new procedure to determine the durations of cell cycle phases is based on th autoradiography of labeled nuclei and a standard chemical determination of DNA content per cell. It has been used to study the cell cycle timing of a human established cell line, EUE cells, so far poorly characterized in its kinetic aspects. The cycle phase durations obtained with this method are compared with the DNA frequency profiles determined by flow cytometry and found to agree closely. The relevance of the growth conditions of the exponentially growing cultures for a correct estimation of the cycle phase duration is indicated. Cell size distribution has been shown to vary according to growth condition.

Autoradiography↗
PubMed2005

Leptin inhibits apolipoprotein M transcription and secretion in human hepatoma cell line, HepG2 cells.

Apolipoprotein M (apoM) is a novel apolipoprotein presented mostly in high-density lipoprotein (HDL) in human plasma. Previously we have reported that both leptin and leptin receptor are essential for apoM expression in vivo. The expression of apoM is lower in the leptin deficient (ob/ob) mouse and leptin receptor deficient (db/db) mouse than in the normal mouse. In the present study, however, we demonstrated that supra-physiological concentrations of recombinant leptin significantly inhibited apoM transcription and secretion in the human hepatoma cell line, HepG2 cells. Both Northern blotting and real-time RT-PCR were applied into the analyses of apoM mRNA levels, and compatible data were obtained. The inhibitory effect of leptin on apoM mRNA levels in HepG2 cells is dose dependent, i.e. 100 ng/mL of leptin decreased apoM mRNA levels by 30%, and 500 ng/mL of leptin decreased apoM mRNA levels about 50%. Even at a physiological concentration of leptin (10 ng/mL), apoM expression was decreased, and in parallel, the secretion of apoM into the medium was also decreased. Furthermore, we examined apoAI, apoB and apoE by Northern blotting analyses. The results demonstrated that leptin does not significantly influence the expressions of apoAI, apoB and apoE in HepC2 cells, suggesting that leptin has a specific regulatory effect on hepatic apoM transcription and secretion in vitro. The mechanism on the contradictory effects of leptin on apoM expression in vivo and in vitro needs further investigation.

Animals↗
PubMed2003

Both IL-4 and IL-13 inhibit the TNF-alpha and IFN-gamma enhanced MDC production in a human keratinocyte cell line, HaCaT cells.

BACKGROUND: Macrophage-derived chemokine (MDC) is a Th2 type chemokine and its receptor CC chemokine receptor 4 (CCR4) is preferentially expressed on Th2 cells. Recent reports demonstrated that MDC is expressed not only by macrophages, dendritic cells and lymphocytes, but also by cultured human keratinocytes (KCs). However, the regulation of MDC production in KCs by various cytokines has not been well documented. OBJECTIVE: In this study, we investigated how Th1/Th2 cytokines regulate MDC production in a human KC cell line, HaCaT cells. METHODS: HaCaT cells were cultured with or without various cytokines for 24 h and RT-PCR was performed using these cells to evaluate MDC mRNA levels. ELISA was carried out using supernatant of HaCaT cells to calculate secreted MDC protein levels. RESULTS: MDC mRNA was weakly expressed in HaCaT cells, and upon stimulation with TNF-alpha or IFN-gamma, MDC expression was strongly upregulated. The supernatant MDC levels when stimulated with TNF-alpha or IFN-gamma were significantly higher than those without stimulation, and were synergistically increased when stimulated with a combination of TNF-alpha and IFN-gamma. Both interleukin-4 (IL-4) and IL-13 inhibited TNF-alpha and IFN-gamma enhanced MDC production in HaCaT cells in a dose-dependent manner. CONCLUSION: Th2-type cytokines IL-4 and IL-13 downregulate the production of MDC, a Th2 type chemokine, by KCs. This may partially contribute to maintaining Th1/Th2 balance in inflammatory skin diseases like atopic dermatitis.

Anti-Inflammatory Agents↗
PubMed1985

[Establishment of a new human endometrial adenocarcinoma cell line, Ishikawa cells, containing estrogen and progesterone receptors].

A new human endometrial adenocarcinoma cell line, Ishikawa cells, was established from an endometrial adenocarcinoma from a 39-year-old woman and has been maintained in vitro for more than 3 years. The cells were found to form a monolayer in a mosaic fashion and to tend to pile up. Population doubling time was calculated to be about 36, 29 and 27 hours at the 9th, 40th and 50th generations, respectively. The modal chromosomal number of the cells fell in a diploid range. Histology of the tumor induced in athymic nude mice showed it to be a well differentiated adenocarcinoma which closely resembled the original human tumor. Estrogen receptor and progesterone receptor were demonstrated to occur not only in the induced tumor in athymic nude mice but also in in vitro culture cells. From the fact that the cell growth was maintained in an estrogen-free medium, it appeared that the cells had no estrogen dependency.

Adenocarcinoma↗
PubMed2005

Human embryonic stem cells: towards therapies for cardiac disease. Derivation of a Dutch human embryonic stem cell line.

Cell transplantation is being discussed as a potential therapy for multiple disorders caused by loss or malfunction of single or at most a few cell types. These include diabetes, Parkinson's disease and myocardial infarction or cardiac failure. However, it is not yet clear whether cells from adult tissues ('adult stem cells') or embryos ('embryonic stem cells') will prove to be the most appropriate replacement cells; most likely, each disease will have its own preferred source. This study presents the background to this discussion and the current state of research in replacement of cardiac tissue, with focus on recent developments using human embryonic stem cells. It also describes a new human embryonic stem cell (HESC) line, NL-HESC1, the first to be derived in the Netherlands, and shows that it forms cardiac cells in a manner comparable with that of hES2 and hES3 cells grown in the same laboratory.

Animals↗
PubMed1977

Separation of cells containing R-type virus-like particles from a simian virus 40-induced hamster tumor cell line.

Cells derived from a simian virus 40-induced hamster fibrosarcoma were separated into two distinct cell bands of differing buoyant densities. The lighter cell band or fraction (F1) had a buoyant density range of 1.025-1.032 g/ml and comprised 3.8% of the total cells applied to the gradient, whereas the heavier cell fraction (F2) had a buoyant density range of 1.054-1.074 g/ml and comprised 95.3% of the total cells applied. Both cell fractions were tumorigenic and did not differ greatly in cell type, viability, mitotic index, or their ability to incorporate [3H]thymidine. However, ultrastructurally, the F1 cells contained R-type virus-like particles within dilated intracisternal spaces and exhibited cytoplasmic vacuoles. In the F2 cells, few detectable R-type particles and cytoplasmic vacuoles were revealed by electron microscopy. The F2 cells demonstrated a twofold greater ability to incorporate [14C]protein hydrolysate into proteins than did the F1 cells.

Cell Line↗
PubMed1981

The extent of histone acetylation induced by butyrate and the turnover of acetyl groups depend on the nature of the cell line.

Cells possessing widely different physiological and morphological features have been treated with substances known to stimulate the differentiation of erythroleukemia cells. Only short fatty acids are capable of causing a hyperacetylation of the core histones and of enhancing the level of an H1-like protein in Chinese hamster ovary cells. While the time courses of a butyrate-mediated acetylation are similar for all cells, the maximum histone acetyl contents are much higher for the transformed cell of a given type. A withdrawal of butyrate rapidly (within 45 min) gives rise to a 'hypoacetylated state' for fibroblasts and transformed fibroblast (epithelial) cells from which there is a slow recovery. Lymphoid cells, on the other hand, display a marked persistance of the highly acetylated forms of histone H4.

Acetylation↗
PubMed1969

Response of simian virus 40-transformed cell lines and cell hybrids to superinfection with simian virus 40 and its deoxyribonucleic acid.

Whereas normal human and monkey cells were susceptible both to intact simian virus 40 (SV40) and to SV40 deoxyribonucleic acid (DNA), human and monkey cells transformed by SV40 were incapable of producing infectious virus after exposure to SV40, but displayed susceptibility to SV40 DNA. On the other hand, mouse and hamster cells, either normal or SV40-transformed, were resistant both to the virus and to SV40 DNA. Hybrids between permissive and nonpermissive parental cells revealed a complex response: whereas most hybrids tested were resistant, three of them produced a small amount of infectious virus upon challenge with SV40 DNA. All were resistant to whole virus challenge. The persistence of infectious SV40 DNA in permissive and nonpermissive cells up to 96 hr after infection was ascertained by cell fusion. The decay kinetics proved to be quite different in permissive and nonpermissive cells. Adsorption of SV40 varied widely among the different cell lines. Very low adsorption of SV40 was detected in nonsusceptible cells with the exception of the mKS-BU100 cell line. A strong increase in SV40 adsorption was produced by pretreating cells with polyoma virus. In spite of this increased adsorption, the resistance displayed by SV40-transformed cells to superinfection with the virus was maintained.

Adsorption↗
PubMed2004

Human cytomegalovirus protects multiple myeloma cell line KM3 cells from apoptosis induced by growth factor withdrawal.

BACKGROUND: There is a higher rate of cytomegalovirus (CMV) reactivation in patients with multiple myeloma after an autologous stem cell transplantation, but no attention has been given thus far to a possible pathogenetic interplay between CMV and multiple myeloma. CMV can infect many kinds of cells, and CMV infection has been shown to inhibit apoptotic responses in several cell systems. In this study the authors investigated the alterations in apoptosis in the multiple myeloma cell line KM3 after infection with CMV and proposed a possible mechanism. METHODS: KM3 cells were infected with 100, 10, or 1 TCID50 of CMV and then cultured in serum-free RPMI 1640. An RT-PCR-based assay was used to detect mRNA expression of CMV-IE, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and IL-6 in CMV-infected and mock-infected cells. Flow cytometry was used to detect apoptotic cells. CMV particles and apoptotic cells were also examined with an electron microscope. RESULTS: CMV-infected KM3 cells clearly expressed immediate early (IE) antigen mRNA when compared to uninfected cells, and there were fewer apoptotic cells among cells treated with 100 or 10 TCID50 of CMV after culturing in serum-free RPMI 1640. CMV particles were observable in infected cells under an electron microscope. Expression of IL-6 mRNA increased after infection. CONCLUSION: CMV can infect the multiple myeloma cell line KM3, inhibit the apoptotic response in these cells after apoptosis induction in serum-free culture, and increase the expression of IL-6 mRNA.

Apoptosis↗
PubMed2005

Constitutive activation of STAT proteins in the HDLM-2 and L540 Hodgkin lymphoma-derived cell lines supports cell survival.

Survival and proliferation of Hodgkin lymphoma (HL) cells are influenced by many cytokines produced by different cell types in the lymph node microenvironment. STAT, family of transcription factors, are key mediators of cytokine signaling and their perturbation contributes to various human diseases. Electrophoretic mobility shift and phosphoprotein immunoblotting analyses were used to study STAT activation in HL cell lines. We thus observed high levels of constitutively activated STAT1, 3, 5 and 6 in HDLM-2 and L540 cells, which could be correlated with JAK kinase activation. In contrast KM-H2 cells did not display STAT activation. Preventing constitutive STAT activation by specific JAK kinases inhibitors induced apoptosis of HL cell lines and was associated with a strong decrease in the expression of the anti-apoptotic genes IAP-1, IAP-2, Bcl-xL, Bfl1 and Traf1. Silencing of JAKs by specific siRNAs also induced apoptosis of HL cells. Altogether, these results suggest that aberrant STAT activation in Hodgkin cells may promote cell survival and as a consequence facilitate oncogenic transformation.

Apoptosis↗
PubMed1989

Mode of action of erythropoietin (Epo) in an Epo-dependent murine cell line. II. Cell cycle dependency of Epo action.

Erythropoietin (Epo), a glycoprotein hormone, regulates the proliferation and differentiation of committed erythroid progenitor cells. We investigated the effect of Epo on the kinetics of an Epo-dependent cell line (DA-1ER), which was cloned from the murine interleukin 3-dependent cell line, DA-1. Flow cytometry and [3H]thymidine incorporation were used to analyze the cell cycle. Removal of Epo from the culture medium resulted in the accumulation of the cells in the G1 phase. Eighteen hours after the removal of Epo, 75%-80% of the cells were arrested in G1 phase. Readdition of Epo to these quiescent cells allowed them to progress from the G1 to the S phase with a lag period of 10 h. Epo was required throughout the lag period in order to achieve maximal DNA synthesis. When the cells were arrested in the G2/M phase or the G1/S interphase by colcemid and thymidine, respectively, and then released from the arrest, they could complete the cell cycle in the absence of Epo. These findings suggest that Epo is only required in the G1 phase for the cells to progress through the cell cycle.

Animals↗