Fas and Fas Ligand Interaction Is Necessary for Human Osteoblast Apoptosis

Kawakami, Atsushi; Eguchi, Katsumi; Matsuoka, Naoki; Tsuboi, Masahiko; Koji, Takehiko; Urayama, Satoshi; Fujiyama, K.; Kiriyama, Takeshi; Nakashima, Tomoki; Nakane, Paul K.; Nagataki, Shigenobu

doi:10.1359/jbmr.1997.12.10.1637

Cited by 77 publications

(53 citation statements)

References 32 publications

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“…46 A predominant pathway of apoptosis in calvarial osteoblasts. 20,21,47,48 and brain 31,[49][50][51] is the Fas mediated pathway. In this pathway, Fas-L activates the Fas receptor to trigger several signaling cascades including Fas-associated death domain (FADD) protein, receptor interacting protein (RIP), or Fas death domain-associated protein (DAXX) and eventually leading to cell death [52][53][54][55][56] Previously, we have reported an upregulation of Fas antigen by overexpression of Nell-1 in MC3T3-E1 osteoblasts in culture.…”

Section: Discussionmentioning

confidence: 99%

“…19 Furthermore, in vitro and in vivo studies have demonstrated that signaling through the CD95/ Fas pathway resulted in increases apoptosis in human and murine osteoblasts. [20][21][22] We previously reported the isolation and identification of a novel gene, NELL-1, in human unilateral coronal craniosynostosis (CS) 23 (concurrently identified by Watanabe et al 24 ). NELL-1 is a secretory protein containing 810 amino acids.…”

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Nell-1 induces acrania-like cranioskeletal deformities during mouse embryonic development

Zhang

Cowan

Jiang

et al. 2006

Laboratory Investigation

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We previously reported NELL-1 as a novel molecule overexpressed during premature cranial suture closure in patients with craniosynostosis (CS). Nell-1 overexpression also results in premature suture closure/ craniosynostosis in newborn transgenic mice. On a cellular level, increased levels of Nell-1 induce osteoblast differentiation and apoptosis. In this report, mice over-expressing Nell-1 were examined during embryonic development as well as shortly after birth for further analysis of craniofacial defects including neural tube defects (NTDs). The results demonstrated that overexpression of Nell-1 could induce acrania at relatively late gestation stage (E15.5) in mouse embryos, through massive apoptosis in calvarial osteoblasts and neural cells. The induced apoptosis was associated with an increase in Fas and Fas-L production. In addition, transgenic E15.5 and newborn transgenic mice with the CS phenotype displayed distortion of the chondrocranium associated with premature hypertrophy and increased apoptosis of chondrocytes. These findings were also verified in vitro with primary chondrocytes transduced with AdNell-1. In conclusion, Nell-1 overexpression can induce craniofacial anomalies associated with neural tube defects during embryonic development and may involve mechanisms of massive apoptosis associated with the Fas/Fas-L signaling pathway. NELL-1: used when describing the human gene; NELL-1: used when describing the human protein; Nell-1: used when describing the rodent gene; Nell-1: used when describing the rodent protein Laboratory Investigation (2006) 86, 633-644.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Nell-1 induces acrania-like cranioskeletal deformities during mouse embryonic development

Zhang

Cowan

Jiang

et al. 2006

Laboratory Investigation

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“…We examined the expression of pro-caspase-8, procaspase-3, and FasL in cultured thyrocytes by Western blotting as previously described (Kawakami et al, 1997a). In brief, treated thyrocytes were collected and lysed by the addition of lysis buffer (50 mM Tris buffer, pH 8, 150 mM NaCl, 0.02% sodium azide, 0.1% SDS, 100 g/ml PMSF, 1 g/ml of aprotinin, 1% NP-40, 0.5% sodium deoxycholate) for 20 minutes at 4°C.…”

Section: Expression Of Pro-caspase-8 Pro-caspase-3 and Fasl In Cultmentioning

confidence: 99%

“…Briefly, incubated CD4 ϩ T cells with SEB-pulsed thyrocytes were initially reacted with PE-conjugated anti-CD4 mAb (MBL). After incubation, cells were permeabilized with digitonin, as described previously (Anderson et al, 1990;Kawakami et al, 1996), because the polyclonal anti-FasL antibody used in the detection of FasL by flow cytometer recognized the cytoplasmic portion of FasL (Kawakami et al, 1997a;Hakuno et al, 1996, corresponding to amino acids;41-55). After confirming the adequacy of permeabilization by trypan blue uptake, permeabilized cells were incubated with anti-FasL Ab for 30 minutes on ice.…”

Section: Examination Of Thyrocyte Apoptosis In Fratricide or Suicide mentioning

confidence: 99%

“…After incubation, the plates were centrifuged, and the percentage of specific lysis was calculated as described above. Apoptotic cell death of thyrocytes was further confirmed by Hoechst 33258 dye staining as previously described (Kawakami et al, 1997a). In brief, treated thyrocytes were fixed with 2% glutaraldehyde solution (Wako Pure Chemical Industries, Osaka, Japan) for 10 minutes and stained with 0.2 mM Hoechst 33258 (Wako) to visualize DNA.…”

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CD4+ T Cell-Mediated Cytotoxicity Toward Thyrocytes: The Importance of Fas/Fas Ligand Interaction Inducing Apoptosis of Thyrocytes and the Inhibitory Effect of Thyroid-Stimulating Hormone

Kawakami

Matsuoka

Tsuboi

et al. 2000

Laboratory Investigation

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SUMMARY:The accumulation of activated CD4 ϩ T cells and antigen (Ag)-dependent cellular interactions between thyrocytes and CD4 ϩ T cells have been determined in thyroid gland from patients with Graves' disease. The Fas/Fas ligand (FasL) interaction between antigen-presenting cells and T cells regulates the apoptosis of the former cells triggered by the latter cells. The inhibition of Fas-mediated apoptosis in thyrocytes could be a underlying mechanism of hyperplasia of thyrocytes in patients with Graves' disease. We investigated the potential role of Fas/FasL interaction between thyrocytes and CD4 ϩ T cells in the induction of Fas-mediated apoptosis of the former cells induced by the latter cells. The presence of only a few specific T cells responsive to a putative autoantigen has hampered the investigation of specific T cell activation toward antigen-presenting cells (APCs). Therefore, we used a superantigen, staphylococcal enterotoxin B (SEB), to examine specific T cell activation toward thyrocytes in vitro since it stimulates a large proportion of T cells with particular V␤ elements. Spontaneous apoptosis of thyrocytes in culture was not found even in the presence of various kinds of cytokines. In contrast, a clear induction of Fas-mediated apoptosis by anti-Fas IgM was determined in interferon-␥ (IFN-␥)-stimulated thyrocytes. In addition, a significant cytotoxicity of purified CD4 ϩ T cells toward IFN-␥-stimulated thyrocytes in the presence of SEB was induced, and the addition of anti-HLA-DR and -DQ monoclonal antibodies (mAbs) or blockade of the Fas/FasL interaction reduced this cytotoxicity. FasL expression of CD4 ϩ T cells cocultured with IFN-␥-stimulated thyrocytes in the presence of SEB was clearly induced. Furthermore, the addition of mAbs against CD54 and CD58 inhibited both cytotoxicity and FasL expression of CD4 ϩ T cells. The cytotoxicity of CD4 ϩ T cells toward IFN-␥-stimulated, SEB-pulsed thyrocytes was markedly inhibited when we used thyrocytes cultured with IFN-␥ in the presence of thyroid-stimulating hormone (TSH) as target cells. Our results suggest that 1) CD4 ϩ T cells were activated by thyrocytes expressing MHC class II molecules in an SEB-dependent manner and then expressed FasL. 2) These activated FasL ϩ CD4 ϩ T cells killed thyrocytes by interacting with Fas on thyrocytes and FasL on activated CD4 ϩ T cells. The presence of costimulating molecules such as CD54 and CD58 on thyrocytes was also necessary to generate activated FasL ϩ CD4 ϩ T cells. 3) Since the actions of thyroid stimulating antibody (TSAb) toward thyrocytes are similar to those of TSH, one goitrogenic activity of TSAb may, in part, be due to the inhibitory effect on Fas-mediated apoptosis of thyrocytes triggered by activated CD4 ϩ T cells. (Lab Invest 2000, 80:471-484).

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Expression of Fas ligand in Langerhans' cell histiocytosis: A case report of a boy with multisystem involvement

et al. 1999

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Previous reports of patients with Langerhans' cell histiocytosis have shown characteristics of osteolytic lesion, visceral involvement and organ dysfunction. We report a 2-year-old boy who was diagnosed as Langerhans' cell histiocytosis with a prominent hepatomegaly. X-Radiogram, computed tomography and magnetic resonance imaging revealed the osteolysis of the right iliac bone, the absence of the left eighth rib as well as the right mandible, and an enhancing mass in the left cerebellum. The data of radiography were highly suggestive of Langerhans' cell lineage. The presence of large CD1a-positive mononuclear cells associated with inflammatory cells in peripheral blood smear and bone marrow aspirate further confirmed the diagnosis. In addition, expressions of S100, CD25, CD68, CD80, CD86, and Fas ligand were identified on these cells by immunocytochemical staining. The results indicate that although these cells are activated Langerhans' cells, progression of the disease and the bone destruction could be mediated by the overt FasL expression of the cells.

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Fas and Fas Ligand Interaction Is Necessary for Human Osteoblast Apoptosis

Cited by 77 publications

References 32 publications

Nell-1 induces acrania-like cranioskeletal deformities during mouse embryonic development

Nell-1 induces acrania-like cranioskeletal deformities during mouse embryonic development

CD4+ T Cell-Mediated Cytotoxicity Toward Thyrocytes: The Importance of Fas/Fas Ligand Interaction Inducing Apoptosis of Thyrocytes and the Inhibitory Effect of Thyroid-Stimulating Hormone

Expression of Fas ligand in Langerhans' cell histiocytosis: A case report of a boy with multisystem involvement

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