Apoptosis

Cohen, John

doi:10.1016/0167-5699(93)90214-6

Cited by 1,100 publications

(644 citation statements)

References 47 publications

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“…Without oblating the classical mechanisms of resistance, for instance the modulation of intracellular drug concentration, enhanced drug metabolism, drug-target ampli®cation or repair of damaged targets, the regulation of apoptosis appears, downstream of the drug-target interactions, as a new concept of drug resistance (Hickman, 1992;Reed, 1995). Apoptosis is a genetically encoded cell death program de®ned by morphological and biochemical events (Cohen, 1993;White, 1996;Williams and Smith, 1993;Wyllie, 1980). This cell death pathway may be in¯uenced by di erent factors such as the tumor cell type, the di erentiation status, growth factors, or oncogenes (reviewed by White, 1996).…”

Section: Introductionmentioning

confidence: 99%

Influence of Bcl-2 overexpression on the ceramide pathway in daunorubicin-induced apoptosis of leukemic cells

et al. 1997

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Section: Introductionmentioning

confidence: 99%

Influence of Bcl-2 overexpression on the ceramide pathway in daunorubicin-induced apoptosis of leukemic cells

et al. 1997

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“…In contrast, cFLIP is a potent inhibitor of CD95-mediated apoptosis, by directly targeting caspase 8 processing at the DISC (9,17,43). Immune system homeostasis is tightly regulated by apoptosis, to eliminate self-reactive lymphocytes and avoid autoimmune reactions (10,11). In the early phase of the immune response, T cells acquire effector functions.…”

Section: Discussionmentioning

confidence: 99%

“…Elimination of T cells during the termination phase of an immune response is called AICD and occurs by apoptosis (9,10). In particular, apoptosis is fundamental for inducing the suicide of supernumerary or damaged cells with high specificity and efficiency and for maintaining T cell homeostasis (11).…”

mentioning

confidence: 99%

NF‐κB protects Behçet's disease T cells against CD95‐induced apoptosis up‐regulating antiapoptotic proteins

Todaro¹,

Zerilli²,

Triolo³

et al. 2005

Arthritis & Rheumatism

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Objective. To determine whether prolongation of the inflammatory reaction in patients with Behçet's disease (BD) is related to apoptosis resistance and is associated with the up-regulation of antiapoptotic factors.Methods. The percentage of cell death was evaluated by flow cytometry in peripheral blood mononuclear cells from 35 patients with BD and 30 healthy volunteers. The expression levels of antiapoptotic factors and NF-B regulatory proteins were measured using Western blotting and immunohistochemical analyses. To down-regulate NF-B nuclear translocation, BD T lymphocytes were exposed in vitro to thalidomide and subjected to transfection with NF-B small interfering RNA.Results. Although CD95 is highly expressed in BD T cells, the absence of sensitivity to CD95-induced apoptosis observed may be attributable to the inhibitory action of antiapoptotic genes. Immunoblot analysis for major antiapoptotic proteins showed considerable upregulation of the short form of cellular FLIP ( Conclusion. Taken together, these results indicate that NF-B contributes to the regulation of the apoptosis-related factors and death receptors leading to apoptosis resistance in BD T cell subsets. Our results suggest that NF-B plays a crucial role in the pathogenesis of BD, and that its pharmacologic control could represent a key strategy in modulating specific immunemediated disease.

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“…Apoptosis is characterized by cell shrinkage, plasma membrane blebbing, nuclear condensation, intact cell membrane, and controlled autodigestion of cells [5,27]. Using annexin V and PI double staining, apoptotic cells can be characterized by positive annexin V staining with exclusion of PI.…”

Section: Bacteria Induced Apoptosis In Chondrocytesmentioning

confidence: 99%

“…Mechanisms of reduced cellularity include cell necrosis and apoptosis. Bacterial toxins and cytokines are known inducers of apoptosis [5,16,27]. However, previous studies about apoptosis in articular cartilage have been focused on synovial apoptosis in rheumatoid arthritis [4,9,18], in endochondral ossification, and in chondrogenesis [1,10-121.…”

Section: Introductionmentioning

confidence: 99%

Signal transduction pathways and apoptosis in bacteria infected chondrocytes

Lee

Yen

Ueng

et al. 2001

Journal Orthopaedic Research

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The mechanism underlying chronic destructive arthropathy after pyogenic arthritis is not clear. This study evaluated the role of apoptosis in Staphylococcus aureus infected human articular chondrocytes and investigated the signal transduction pathways activated by bacterial infection. Chondrocytes cultured in monolayer were challenged with bacteria for 6 h and were analyzed after incubation for 2, 18, and 24 h. Chondrocytes showed morphologic and biochemical evidences of apoptosis after infection and the following incubation period. Although treatment with extensive washing and vancomycin could ameliorate the amount of apoptosis from 31% to 15% at 2 h, from 48% to 23% at 18 h, and from 58% to 33% at 24 h, the infected samples with treatment still had higher amount of apoptosis than the un-infected controls (ANOVA P < 0.001). Accompanying with the increasing amount of apoptosis, the caspase activity was upregulated in bacteria infected samples and remained high in samples with treatment (ANOVA P < 0.05).Signal transduction pathways activated by bacterial infection were assessed by co-transfection technique. After infection, the c-Jun N-terminal kinase, extracellular signal-regulated kinase, and cyclic AMP-dependent protein kinase activities were elevated by 7.6-, 7.3-, and 3.2-fold, respectively, compared to the uninfected controls. The data support the hypothesis that human chondrocytes will undergo apoptosis after infection by a single organism. Apoptosis and activated intracellular kinase activities may be related to the pathogenesis of post-infectious destructive arthropathy.

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Apoptosis

Cited by 1,100 publications

References 47 publications

Influence of Bcl-2 overexpression on the ceramide pathway in daunorubicin-induced apoptosis of leukemic cells

Influence of Bcl-2 overexpression on the ceramide pathway in daunorubicin-induced apoptosis of leukemic cells

NF‐κB protects Behçet's disease T cells against CD95‐induced apoptosis up‐regulating antiapoptotic proteins

Signal transduction pathways and apoptosis in bacteria infected chondrocytes

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