The baculovirus antiapoptotic p35 gene also functions via an oxidant-dependent pathway

Sah, Nand K.; Taneja, Tarvinder K.; Pathak, Niteen; Begum, Rasheedunnisa; Athar, Mohammad; Hasnain, Seyed E.

doi:10.1073/pnas.96.9.4838

Cited by 52 publications

(35 citation statements)

References 42 publications

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“…Several groups have recently shown that fibers/particles induce apoptosis, the extent of which is reduced in the presence of various cellular antioxidants such as catalase and N-acetylcysteine (37). Further, antiapoptotic proteins such as Bcl-2 and baculovirus protein p35 are well known for their antioxidant properties (38,39). chelators and OH radical scavengers has also been demonstrated (41).…”

Section: Discussionmentioning

confidence: 99%

Evidence that ultrafine titanium dioxide induces micronuclei and apoptosis in Syrian hamster embryo fibroblasts.

Rahman

Lohani

Dopp

et al. 2002

Environ Health Perspect

355

218

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Inhaled ultrafine titanium dioxide (UF-TiO2) particles cause pronounced pulmonary inflammation, in contrast to fine TiO2. Previous studies provide evidence for the production of reactive oxygen species by alveolar macrophages, after overloading with UF-TiO2 particles and cytotoxicity of UF-TiO2 in rat lung alveolar macrophages. UF-TiO2 also causes pulmonary fibrosis and lung tumors in rats. UF-TiO2 particles are photogenotoxic, but in general, information on the genotoxicity of UF-TiO2 is still limited. We studied the potential of UF-TiO2 (particle size less than or equal to 20 nm) and fine TiO2 (particle size > 200 nm) to induce chromosomal changes, which can be monitored by the formation of micronuclei (MN) in Syrian hamster embryo (SHE) cells. We also analyzed UF-TiO2-treated cells for apoptosis induction. The MN assay revealed a significant increase in MN induction (p less than or equal to 0.05) in SHE cells after treatment with UF-TiO2 (1.0 micro g/cm2) for 12 hr (mean, 24.5 MN/1,000 cells), 24 hr (mean, 31.13 MN/1,000 cells), 48 hr (mean, 30.8 MN/1,000 cells), 66 hr (mean, 31.2 MN/1,000 cells), and 72 hr (mean, 31.3 MN/1,000 cells). Bisbenzimide staining of the fixed cells revealed typical apoptotic structures (apoptotic bodies), and the apoptosis-specific "DNA ladder pattern" resulting from internucleosomal cleavage was identified by gel electrophoresis. Furthermore, transmission electron microscopy of the exposed cells revealed the typical chromatin compaction of apoptosis.

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Section: Discussionmentioning

confidence: 99%

Evidence that ultrafine titanium dioxide induces micronuclei and apoptosis in Syrian hamster embryo fibroblasts.

Rahman

Lohani

Dopp

et al. 2002

Environ Health Perspect

355

218

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“…It has previously been reported that the baculoviral caspase inhibitor, p35, was not only capable of preventing apoptosis in retinal degenerative Drosophila mutants, but also of maintaining visual functionality. 61 Interestingly, a recent report has attributed an anti-oxidant property to p35 62 suggesting that cell survival in these retinal degenerative mutants may not only require inhibition of the effectors of the cell death machinery, but also of the initiating signals. In light of this view, and as our findings demonstrate, the use of antioxidants may be of more therapeutic benefit in the prevention of retinal degeneration in RP than inhibitors of the caspases.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress induces caspase-independent retinal apoptosis in vitro

2000

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Apoptosis is the mode of cell death in retinitis pigmentosa (RP), a heterogeneous group of retinal degenerations. The activation of the caspase proteases forms a pivotal step in the initiation and execution phase of apoptosis in many cells. Inhibition of caspases has been reported to prevent apoptosis in many model systems. However, we demonstrate the absence of caspase activation during retinal cell apoptosis in vitro which involves phosphatidylserine (PS) externalisation, DNA nicking and cell shrinkage. In addition, zVAD-fmk, DEVD-CHO and BD-fmk, inhibitors of the caspases, were unable to alter the characteristics or kinetics of apoptosis, implying that retinal cell death in vitro follows a caspase-independent pathway. We have previously demonstrated the ability of reactive oxygen species (ROS) to act as mediators of retinal cell apoptosis in vitro as well as the ability of antioxidants to prevent retinal cell apoptosis. Here we demonstrate the oxidative inactivation of caspases in this model of retinal apoptosis and provide evidence for an oxidative stress driven cell death pathway that does not involve caspase activity and which retains key features of apoptotic cell death. Furthermore, our data indicates that apoptotic events such as PS exposure, DNA nicking and cell shrinkage may occur independently of caspase activity. Cell Death and Differentiation (2000) 7, 282 ± 291.

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“…The experiment was done as mentioned previously (25,26). Briefly, after incubation, cells were washed twice with ice-cold PBS and re-suspended in lysis buffer (1% Triton X-100, 0.32 M sucrose, 5 mM EDTA, 1 mM phenylmethylsulfonyl fluoride, 1.0 g/ml aprotinin, 1.0 g/ml leupeptin, 2 mM dithiothreitol, 10 mM Tris-HCl, pH 8) for 5 min at 4°C followed by protein determination with BCA method (Pierce).…”

Section: The Induction Of the Expression Of Pro-apoptotic And Antiapomentioning

confidence: 99%

Distinct Role of CD80 and CD86 in the Regulation of the Activation of B Cell and B Cell Lymphoma

Suvas¹,

Singh²,

Sahdev³

et al. 2002

Journal of Biological Chemistry

216

205

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To date, not much has been known regarding the role of CD80 and CD86 molecules in signaling of B cells. The CD28/CTLA4 ligands, CD80 (B7-1) and CD86 (B7-2), are expressed on the surface of freshly isolated splenic B cells, and their expression is up-regulated by lipopolysaccharides. In the present study, we have investigated whether signaling via CD80/CD86 could alter the proliferation and immunoglobulin synthesis of B cells. Splenic B cells were stimulated with lipopolysaccharides in the presence of anti-B7-1 (16-10A1) and anti-B7-2 (GL1) monoclonal antibodies (mAbs). Exciting features observed during the study were that cross-linking of CD86 with GL1 enhanced the proliferation and production of IgG1 and IgG2a isotypes. In contrast, anti-B7-1 (16-10A1) mAb could efficiently block the proliferation and production of IgG1 and IgG2a. Furthermore, GL1 mAb could also induce the secretion of IgG isotypes from B cell lymphomas. Importantly, 16-10A1 could retard the growth of lymphomas and favored the up-regulation of pro-apoptotic molecules caspase-3, caspase-8, Fas, FasL, Bak, and Bax and down-regulation of antiapoptotic molecule Bcl-x(L). In contrast, GL1 augmented the level of anti-apoptotic molecules Bcl-w and Bcl-x(L) and decreased the levels of pro-apoptotic molecule caspase-8, thereby providing a novel insight into the mechanism whereby triggering through CD80 and CD86 could deliver regulatory signals. Thus, this study is the first demonstration of a distinct signaling event induced by CD80 and CD86 molecules in B cell lymphoma. Finally, the significance of the finding is that CD80 provided negative signal for the proliferation and IgG secretion of normal B cells and B cell lymphomas. In contrast, CD86 encouraged the activity of B cells.Evidence from a variety of studies has suggested that the B cell contact with T helper cells is important for its optimal activation and responsiveness to cytokines during Ig secretion (1-3). Contact between B and T cells can be mediated by antigen presentation, as well as antigen-independent cell interaction by molecules known as adhesion (LFA-1, LFA-3, ICAM-1, etc.) and costimulatory molecules (CD80, CD86, CD40, etc.) (3-7). Signals from T cells induce two opposite fates in B cells: clonal expansion of B cells that bind specifically to foreign antigens and clonal deletion of equivalent B cells that bind self-antigen. The role of costimulatory molecules is very well established in the activation of T cells (3), but nothing has been determined definitively about how these molecules operate in the activation and differentiation of B cells (8 -10).The best defined co-stimulators to date are two structurally related proteins, . Both of these play a major role in providing costimulation to T cells, leading to their proliferation, cytokine production, and development of effector functions. CD80 and CD86 could also serve as counter-receptors that transduce distinct signal to the antigen-presenting cells upon engagement by CD28 or CTLA-4. The intracellular domains of CD80 and CD86 are ...

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The baculovirus antiapoptotic p35 gene also functions via an oxidant-dependent pathway

Cited by 52 publications

References 42 publications

Evidence that ultrafine titanium dioxide induces micronuclei and apoptosis in Syrian hamster embryo fibroblasts.

Evidence that ultrafine titanium dioxide induces micronuclei and apoptosis in Syrian hamster embryo fibroblasts.

Oxidative stress induces caspase-independent retinal apoptosis in vitro

Distinct Role of CD80 and CD86 in the Regulation of the Activation of B Cell and B Cell Lymphoma

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