Silencing of Fas-associated Death Domain Protects Mice from Septic Lung Inflammation and Apoptosis

Matsuda, Naoyuki; Yamamoto, Seiji; Takano, K.; Kageyama, Shun‐Ichiro; Kurobe, Yusuke; Yoshihara, Yasunori; Takano, Yasuo; Hattori, Yoshiyuki

doi:10.1164/rccm.200804-534oc

Cited by 79 publications

(62 citation statements)

References 42 publications

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“…Cell death evoked by cytokine challenge was remarkable, and the increase in level of cleaved cytokeratin 18 strongly suggested the substantial involvement of caspase-dependent apoptosis. These results are compatible with other reports arguing that apoptosis pathways are activated in septic ALI experimentally or clinically (5)(6)(7)11,40,41).…”

Section: Discussionsupporting

confidence: 93%

Analysis of cytotoxicity induced by proinflammatory cytokines in the human alveolar epithelial cell line A549

et al. 2012

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Section: Discussionsupporting

confidence: 93%

Analysis of cytotoxicity induced by proinflammatory cytokines in the human alveolar epithelial cell line A549

et al. 2012

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“…Although Fas is constitutively expressed in a variety of cell types, the role of Fas has also been evoked recently in apoptosis of various cell types in response to certain stimuli; [32][33][34] ultraviolet irradiation, viral infection, and chemotherapeutic agents effectively increase Fas transcription and, in turn, upregulation of Fas is involved in apoptotic cell death. 35 We also provide further evidence that nanosized TiO . In response to stimuli such as etoposide, staurosporine, transforming growth factor-β, and ultraviolet irradiation, which require a mitochondria-dependent pathway for apoptosis, Bax is activated, translocated to the outer membrane of mitochondria, oligomerized therein, 36,37 and, mitochondrial membranes are permeabilized, thereby releasing mitochondrial apoptogenic molecules into the cytosol.…”

Section: P25-70supporting

confidence: 59%

Titanium dioxide induces apoptotic cell death through reactive oxygen species-mediated Fas upregulation and Bax activation

Yoo¹,

Yoon²,

Kwon³

et al. 2012

IJN

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Background: Titanium dioxide (TiO 2 ) has been widely used in many areas, including biomedicine, cosmetics, and environmental engineering. Recently, it has become evident that some TiO 2 particles have a considerable cytotoxic effect in normal human cells. However, the molecular basis for the cytotoxicity of TiO 2 has yet to be defined. Methods and results:In this study, we demonstrated that combined treatment with TiO 2 nanoparticles sized less than 100 nm and ultraviolet A irradiation induces apoptotic cell death through reactive oxygen species-dependent upregulation of Fas and conformational activation of Bax in normal human cells. Treatment with P25 TiO 2 nanoparticles with a hydrodynamic size distribution centered around 70 nm ) together with ultraviolet A irradiation-induced caspase-dependent apoptotic cell death, accompanied by transcriptional upregulation of the death receptor, Fas, and conformational activation of Bax. In line with these results, knockdown of either Fas or Bax with specific siRNA significantly inhibited TiO 2 -induced apoptotic cell death. Moreover, inhibition of reactive oxygen species with an antioxidant, N-acetyl-L-cysteine, clearly suppressed upregulation of Fas, conformational activation of Bax, and subsequent apoptotic cell death in response to combination treatment using TiO 2 P25-70 and ultraviolet A irradiation. Conclusion:These results indicate that sub-100 nm sized TiO 2 treatment under ultraviolet A irradiation induces apoptotic cell death through reactive oxygen species-mediated upregulation of the death receptor, Fas, and activation of the preapoptotic protein, Bax. Elucidating the molecular mechanisms by which nanosized particles induce activation of cell death signaling pathways would be critical for the development of prevention strategies to minimize the cytotoxicity of nanomaterials.

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“…Fas is a trans-membrane protein of tumor necrosis factor receptor superfamily (Inoue et al, 2009;Matsuda et al, 2009;Akimzhanov et al, 2010;Liedtke and Trautwein, 2012) and is expressed extensively on the cytoplasmic membrane. When Fas is bound to its ligand, the apoptotic signal may be transferred to the cells.…”

Section: Fas Expression Of Mg63 By Immunocytochemistrymentioning

confidence: 99%

Marsdenia tenacissima extract sensitizes MG63 cells to doxorubicin-induced apoptosis

et al. 2014

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ABSTRACT. Marsdenia tenacissima extract (MTE) is a new platederived biotechnology product that is frequently used, but occasionally reported, in the field of chemotherapy. In this study, we assessed the antitumor activity and related mechanisms of MTE by various biotechnological methods. The survival rates of MG63 osteosarcoma cells treated with MTE and doxorubicin were measured, individually or jointly, and the changes in cellular shape, apoptotic rates, and Fas expression were observed. The results indicated that combination of MTE and doxorubicin up-regulated Fas expression and induced apoptosis. The survival rate of combined application of 50 mg/mL MTE and 1 µg/mL doxorubicin was significantly lower than that of the individual application (P < 0.01). Other biotechnology methods also showed an apoptosis-inducing effect of combined application that was much stronger than individual application. All of these results suggested that MTE may promote the effects of doxorubicin chemotherapy, perhaps related to the up-regulation of Fas expression in tumor cells.

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Silencing of Fas-associated Death Domain Protects Mice from Septic Lung Inflammation and Apoptosis

Abstract: These results indicate the pathophysiologic significance of the death receptor apoptotic pathway, including FADD, in septic ALI and the potential usefulness of FADD siRNA for gene therapy of the septic syndrome.

Cited by 79 publications

References 42 publications

Analysis of cytotoxicity induced by proinflammatory cytokines in the human alveolar epithelial cell line A549

Analysis of cytotoxicity induced by proinflammatory cytokines in the human alveolar epithelial cell line A549

Titanium dioxide induces apoptotic cell death through reactive oxygen species-mediated Fas upregulation and Bax activation

Marsdenia tenacissima extract sensitizes MG63 cells to doxorubicin-induced apoptosis

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