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  • 1995-1999  (23)
  • 1900-1904
  • 1999  (23)
  • Apoptosis  (23)
  • 1
    Electronic Resource
    Electronic Resource
    Cell cycle regulation and induction of apoptosis by IL-6 variants on the multiple myeloma cell line XG-1 (1999)
    Springer
    Annals of hematology 78 (1999), S. 13-18 
    Details
    ISSN: 1432-0584
    Keywords: Key words IL-6 variants ; Cell cycle ; Apoptosis ; Multiple myeloma ; Cell line
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Interleukin-6 (IL-6) serum levels and the proliferative activity of bone marrow plasma cells have been described as important prognostic factors for survival duration in multiple myeloma (MM) patients. Since growth of neoplastic plasma cells is frequently promoted by IL-6, inhibition of its activity has been considered for the management of MM patients. With a similar rationale, IL-6 variants characterized by wild-type or increased affinity for the ligand-specific IL-6 α receptor chain and reduced ability to bind and/or dimerize the gp 130 chain have recently been generated. In the present study, the antiproliferative effects of the variants Sant1, Sant5, and Sant7, characterized by increasing antagonistic activity, were investigated by means of a detailed cell kinetic and apoptotic analysis of the IL-6-dependent MM XG-1 cell line. A significant reduction in the mean percent of XG-1 cells in active S-phase (DNA/bromodeoxyuridine incorporation) from 41% to 28.1% (p=0.04), 25.8% (p=0.04), and 15.3% (p=0.02), respectively, was observed using Sant1, Sant5, and Sant7. These effects were confirmed using the acridine-orange (AO) flow-cytometric technique, which showed a similar reduction of S-phase (34.2% of baseline value) in the presence of Sant1, Sant5, and Sant7, as well as a significant G1b arrest (from 44.5% to 47.6%, 48%, and 64.9%). Furthermore, IL-6 variants were capable of down-regulating the G1 cell cycle regulatory protein cyclin D1 expression. Cell cycle effects were coupled with a significant increase of apoptosis, measured by the AO and the terminal deoxynucleotidyl transferase assays, from 12.9% (control culture with IL-6) to 21.2% (Sant1), 29.1% (Sant5), and 23.5% (Sant7). These results were comparable to those obtained by depriving XG-1 of recombinant IL-6. Our study documents the antiproliferative activity exerted by IL-6 mutants on the XG-1 cell line, thus supporting the investigation of these molecules on primary MM cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050465
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  • 2
    Electronic Resource
    Electronic Resource
    Molecular pathogenesis of chronic lymphocytic leukemia: factors and signaling pathways regulating cell growth and survival (1999)
    Springer
    Journal of molecular medicine 77 (1999), S. 282-293 
    Details
    ISSN: 1432-1440
    Keywords: Key words Chronic lymphocytic leukemia ; Apoptosis ; Cell growth ; Signaling ; Review
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Chronic lymphocytic leukemia is a malignant disease characterized by clonal expansion of relatively mature B-lymphocytes with a high percentage of cells arrested in the nonproliferative G0/G1 cell cycle phase. Possibly reflecting the clinical heterogeneity observed in patients, various signaling pathways may become affected during the initiation and course of this disease. This review discusses frequent alterations concerning proliferative, differentiation-inducing, and apoptotic pathways elucidated in the recent years that have improved our understanding of this disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001090050351
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  • 3
    Electronic Resource
    Electronic Resource
    Oligodendroglial degeneration in distemper: apoptosis or necrosis? (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 279-287 
    Details
    ISSN: 1432-0533
    Keywords: Key words Canine distemper virus ; Oligodendrocytes ; Apoptosis ; Necrosis ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Canine distemper virus (CDV) causes a multifocal demyelinating disease in dogs. It was previously shown that the initial demyelinating lesions are directly virus induced since a correlation between the occurrence of demyelination and CDV replication in white matter cells was observed. During the course of infection oligodendrocytes undergo distinct morphological alterations, partly due to a restricted CDV infection of these cells, and eventually disappear from the lesions. This phenomenon has been described in vivo as well as in vitro. However, the reason for the morphological alterations and the following oligodendroglial depletion remained unclear. Since virus infection can induce cell death, it was investigated whether apoptosis or necrosis plays a role in the pathogenesis of demyelination in canine distemper. In brain tissue sections from dogs with acute distemper apoptotic cells were not detected within the demyelinating lesions using morphological and biochemical cell death criteria. In chronic distemper, apoptotic cells – presumably inflammatory cells – were seen within the perivascular cuffs. These in vivo findings were correlated to the in vitro situation using CDV-infected primary dog brain cell cultures as well as Vero cells. Infection with culture-adapted CDV lead to massive necrosis but not to apoptosis. After infection with virulent CDV neither apoptosis nor necrosis was a predominant feature in either culture system. These findings suggest that virus-induced demyelination in canine distemper is not the direct consequence of apoptosis or necrosis. It is speculated that another mechanism must be responsible for the observed morphological alterations of oligodendrocytes, ultimately leading to demyelination.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050986
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  • 4
    Electronic Resource
    Electronic Resource
    Combined use of radioimagers and radioactive 3′OH DNA nick end labelling to quantify apoptosis in cell lines and tissue sections: applications to virus-induced apoptosis (1999)
    Springer
    Apoptosis 4 (1999), S. 169-178 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; β-IMAGER ; dengue virus ; DNA fragmentation ; radioimager μ-IMAGER ; rabie virus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract DNA fragmentation is a key feature of the degradation phase of apoptosis. In this work we have developed an assay, based on radioimager (β-IMAGER and μ-IMAGER) quantification of radioactive nick end labelling (RANEL), which is quantitative, rapid and sensitive to study in vitro and in vivo induced apoptosis. To establish the technique, in vitro apoptosis of T cell lines was induced by stimulation of the Fas receptor; cells were labelled using TdT-mediated [α-33P] dCTP nick end labelling, after which then radioactivity was quantified using a β-IMAGER. We have also shown that the RANEL method can be applied to the quantification and visualisation, by μ-IMAGER analysis, of liver tissue sections from mouse Fas-induced fulminant hepatitis or from Dengue-1 virus infected individuals. Finally, this system has also been used to detect apoptosis induced by rabies virus in Jurkat T cells. These data have established a large field of application for the RANEL assay.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009658522328
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  • 5
    Electronic Resource
    Electronic Resource
    Regulation of cell survival in CD95-induced T cell apoptosis: role of NF-κB/Rel transcription factors (1999)
    Springer
    Apoptosis 4 (1999), S. 179-186 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; CD95 (Fas/APO-1) ; NF-κB/Rel ; T lymphocytes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The activity of NF-κB/Rel transcription factors can inhibit the apoptosis induced by TNF, UV or cancer therapy drugs in a number of cell types, including human T lymphocytes. Furthermore, the NF-κB/Rel inducer, phorbol-12-myristate-13-acetate (PMA), has been reported to suppress the CD95-induced apoptosis of human T lymphocytes. To verify whether the survival-enhancing effect of PMA required NF-κB/Rel activity, we generated two Jurkat cell sublines (AL.7 and AL.8) transfected with a pCMV4-IκBα construct, and two (AL.3 and AL.5) with the void pCMV4 vector. Compared to wild type, AL.3 and AL.5 cells, the AL.7 and AL.8 sublines displayed markedly lower amounts of NF-κB/Rel nuclear complexes and a reduced expression of a κB-controlled CAT reporter gene after 1 and 4 h of incubation with PMA, respectively. All the five cell types displayed negligible levels of apoptosis when cultured with medium or PMA alone; when stimulated with the mAb CH-11, the AL.7 and AL.8 sublines displayed apoptotic responses only slightly (〈0.5 fold) higher than control cells. On the other hand, the salvage activity of PMA was partially impaired in the AL.7 and AL.8 sublines. PMA inhibited apoptosis by 〉85% in wild type, AL.3 and AL.5 cells and by 〈60% in the AL.7 and AL.8 sublines; the apoptosis percentages in the mAb CH-11 + PMA cultures of the IκBα-transfected cells were 〉4-fold higher than in control cells. We conclude that the inhibition of the CD95-induced apoptosis by PMA relies on both NF-κB/Rel-dependent and -independent mechanisms. The partial contribution of these nuclear factors to the suppression of apoptosis indicates that the NF-κB/Rel activity can influence the extent of the CD95-induced T cell death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009662606398
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  • 6
    Electronic Resource
    Electronic Resource
    p53-Independent caspase-mediated apoptosis in human leukaemic cells is induced by a DNA minor groove binder with antineoplastic activity (1999)
    Springer
    Apoptosis 4 (1999), S. 39-45 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; caspases ; leukaemic cells ; minor groove binders
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Treatment of HL60 and Jurkat leukaemic cell lines, both not expressing p53, with the new non-covalent DNA minor groove binder α-bromoacryloyl-distamycin (PNU 151807), induces apoptosis as shown either morphologically or by DNA laddering formation. We evaluated the p53-independent mechanisms of activation of apoptosis in these cell systems, by determining the levels of different caspases at different times after treatment with PNU 151807. Through Western blotting analysis we could measure the cleavage of the 110 Kd form of PARP in both HL60 and Jurkat cells and correspondingly the activation of CPP32-caspase 3. The levels of caspase-1 did not change at any time after drug treatment. By using the tetrapeptidic sequence recognized by caspase-3 (DEVD-AMC) or by caspase-1 (YVAD-AMC) linked to fluorogenic substrate, we also demonstrated that only the DEVD sequence was recognized and cleaved after drug treatment, while no significant changes were found for YVAD peptides. PNU 151807-induced DNA fragmentation and DEVD-cleavage were both inhibited by concomitant treatment with the specific inhibitor DEVD-CHO, but not by YVAD-CHO, clearly demonstrating the direct activation of caspase-3-like caspases in the induction of programmed cell death in these cell lines after minor groove binder exposure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009630132087
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  • 7
    Electronic Resource
    Electronic Resource
    Sustained suppression of Fas ligand expression in cisplatin-resistant human ovarian surface epithelial cancer cells (1999)
    Springer
    Apoptosis 4 (1999), S. 271-282 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; chemoresistance ; cisplatin ; Fas ; FasL ; ovarian cancer.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Although cisplatin derivatives are first line chemotherapeutic agents for the treatment of ovarian epithelial cancer, chemoresistance is a major therapeutic problem. Although the cytotoxic effect of these agents are believed to be mediated through the induction of apoptosis, the role of the Fas/FasL system in chemoresistance in human ovarian epithelial cancer is not fully understood. In the present study, we have used cultures of established cell lines of cisplatin-sensitive human ovarian epithelial tumours (OV2008 and A2780-s) and their resistant variants (C13* and A2780-cp, respectively) to assess the role ofFas/FasL system in the chemo-responsiveness of ovarian cancer cells to cisplatin. Cisplatin was effective in inducing the expression of cell-associated Fas and FasL, soluble FasL and apoptosis in concentration and time-dependent fashion in both cisplatin-sensitive cell lines (OV2008 and A2780-s). In contrast, while cisplatin was effective in increasing cell-associated Fas protein content in C13*, it failed to up-regulate FasL (cell-associated and soluble forms) and induce apoptosis, irrespective of concentration and duration of cisplatin treatment. Concentrated spent media from OV2008 cultures after cisplatin treatment were effective in inducing apoptosis in C13* cells which was partly inhibited by the antagonistic Fas monoclonal antibody (mAb) suggesting that the soluble FasL present in the spent media was biologically active. In the resistant A2780-cp cells, neither Fas nor FasL up-regulation were evident in the presence of the chemotherapeutic agent and apoptosis remained low compared to its sensitive counterpart. Activation of the Fas signalling pathway, by addition to the cultures an agonistic Fas mAb, was equally effective in inducing apoptosis in the cisplatin-sensitive (OV2008) and -resistant variant C13*, although these responses were of lower magnitude compared to that observed with cisplatin in the chemosensitive cells. A significant interaction between cisplatin and agonistic Fas mAb was observed in the apoptotic response in OV2008 and C13* when cultured in the presence of both agents. Immunohistochemistry of human ovarian epithelial carcinomas reveals the presence of Fas in low abundance in proliferatively active cells but in high levels in quiescent ones. Although the expression pattern of FasL in the tumour was similar to that of Fas, the protein content was considerably lower. Taken together, these data suggest that the dysregulation of the Fas/FasL system may be an important determinant in cisplatin resistance in ovarian epithelial cancer cells. Our results are also supportive of the notion that combined immuno- and chemo-therapy (i.e., agonistic Fas mAb plus cisplatin) may provide added benefits in the treatment of both chemo-sensitive and -resistant ovarian tumours.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026456926754
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  • 8
    Electronic Resource
    Electronic Resource
    Growth inhibition of experimental pancreatic cancers and sustained reduction in epidermal growth factor receptors during therapy with hormonal peptide analogs (1999)
    Springer
    Journal of cancer research and clinical oncology 125 (1999), S. 444-452 
    Details
    ISSN: 1432-1335
    Keywords: Key words Experimental pancreatic cancer ; Hormonal therapy ; Bombesin antagonist ; Somatostatin analog ; LH-RH antagonist ; EGF receptor ; Apoptosis ; AgNOR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Reduction in receptors for epidermal growth factor (EGF) in cancers appears to be one of the principal mechanisms through which peptide hormone analogs can inhibit tumor growth. In this study, hamsters with nitrosamine-induced pancreatic cancers were treated for 8 weeks with bombesin/gastrin-releasing peptide (GRP) antagonist RC-3095, somatostatin analog RC-160 or the luteinizing hormone-releasing hormone antagonist Cetrorelix, using sustained delivery systems releasing 20, 35 and 20 μg analog/ day respectively. To establish the pattern of changes in the number and affinity of EGF receptors on tumors, groups of animals were sacrificed at regular intervals during therapy. Chronic treatment with RC-3095 or Cetrorelix resulted in an early (day 10) and sustained reduction (71% or 69% respectively) in EGF receptors on pancreatic tumors. In contrast, RC-160 decreased receptor concentration by 60% only after 20 days. Among the histological characteristics of proliferation, the decrease in argyrophilic nucleolar organizer regions, but not apoptotic and mitotic indices, showed a correlation with the fall in EGF receptors. The concentration of the receptors returned to the control level 4 days after cessation of chronic treatment with RC-3095. The effect of single injections of RC-3095, RC-160 and Cetrorelix on EGF receptors was also investigated. RC-160 decreased the number of EGF receptors on pancreatic cancers by 31% 3 h after administration, but the receptors had returned to normal level at 6 h. RC-3095 and Cetrorelix caused a 67% and 59% decline, respectively, in EGF receptors only 6 h after injection and the concentration of receptors remained low for 24 h. Thus, the pattern of down-regulation of EGF receptors in pancreatic cancers appears to depend on the peptide used for therapy. Since the antitumor effect may be the result of the fall in EGF receptors in cancers, information on the time course of changes in these receptors during treatment with these analogs may lead to an improvement in therapeutic regimens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050301
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  • 9
    Electronic Resource
    Electronic Resource
    Oxidation of lipoprotein in injury and repair of obstructive nephropathy (1999)
    Springer
    Clinical and experimental nephrology 3 (1999), S. 254-260 
    Details
    ISSN: 1437-7799
    Keywords: Key words Low density lipoprotein ; Apoptosis ; Malondialdehyde ; TGFβ1 ; Unilateral ureteral obstruction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background. To test the hypothesis that oxidized low density lipoprotein (oLDL) is involved in the renal injury of obstructive nephropathy, male Sprague-Dawley rats weighing 125–150 g were used. Methods. Three days after arrival, the rats were randomly assigned to undergo: (1) sham operation, (2) left unilateral ureteral obstruction (UUO), or (3) reversal of the unilateral ureteral obstruction (R-UUO). Seven days after the reversal operation or 10 days after the sham or UUO procedure, all animals were killed by exsanguination under anesthesia, with blood taken from the abdominal aorta. LDL was prepared by gradient ultracentrifugation and used immedi-ately after isolation. Rat mesangial cells were utilized with an LDL concentration of 100 μg/ml/protein in the media. After 72 h, cell survival was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) method. Cell survival was determined by comparing the optical density between the control wells and the experimental wells. In order to investigate the mechanisms of injury and repair of obstructive nephropathy, data for kidney apoptosis, malondialdehyde (MDA), and transforming growth factor β1 (TGFβ1) mRNA were obtained in the sham-operated, UUO, and R-UUO groups. Results. Our results showed that LDL malondialdehyde during UUO was increased 87% over baseline values (P 〈 0.005). With R-UUO, the oxidized LDL dropped 23% from the peak values during UUO (P 〈 0.005), but was still different from that of the baseline values (P 〈 0.025). Rat mesangial cell survival, after 72 h exposure to oLDL, inversely correlated to oLDL cytotoxicity and showed a 14% drop during UUO compared with sham-operated animals (P 〈 0.01). Cell survival increased 11% after R-UUO (P 〈 0.02) and was not different from control values (P = NS). The apoptotic counts by the TUNEL (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labelling) technique showed significant increases during UUO and a noticeable reduction after R-UUO. Conclusion. Our data support the proposition that UUO stimulates oxidation of LDL. The cytotoxicity of oLDL plays a significant role in the injury of UUO. A decrease in cytotoxicity was associated with the repair in R-UUO. Our observations that apoptosis follows this same pattern, point to the importance of apoptosis in the injury and repair of obstructive nephropathy. Future studies to interrupt these processes of injury may lead to novel treatment modalities in reversing the injury and hastening the repair of obstructive nephropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s101570050044
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  • 10
    Electronic Resource
    Electronic Resource
    Neuronal vacuolation in young Rottweiler dogs (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 192-195 
    Details
    ISSN: 1432-0533
    Keywords: Key words Neuronal vacuolation ; Rottweiler dog ; Bcl-2 ; Bax ; c-Jun ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Neuronal vacuolation, involving the cerebellar roof nuclei, Purkinje cells, selected nuclei of the brain stem, thalamus, Clarke’s column, anterior and posterior horns of the spinal cord, visceral autonomic ganglia and myenteric plexus, as well as axonal degeneration of the white matter of the brain stem, cerebellar pedunculi, dorsolateral columns of the spinal cord and ventral roots of the spinal cord, were observed in two young Rottweiler dogs which were clinically afflicted with hind limb weakness progressing to paraparesia, ataxia, intention tremor, and difficulty in swallowing and barking. The absence of modifications in Bcl-2 and Bax immunoreactivity, a lack of strong c-Jun/AP-1 (N) immunoreactivity in vacuolated cells, and the absence of DNA breaks, as seen with the method of in situ end-labeling of nuclear DNA fragmentation, all suggest that there is no involvement of the apoptotic pathway in vacuolated cells in this new neurodegenerative disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050973
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