Transcription Stimulation of the Fas-encoding Gene by Nuclear Factor for Interleukin-6 Expression upon Influenza Virus Infection

Wada, Naoya; Matsumura, Miho; Ohba, Yoshiki; Kobayashi, Nobuyuki; Takizawa, Takenori; Nakanishi, Yoshinobu

doi:10.1074/jbc.270.30.18007

Cited by 94 publications

(71 citation statements)

References 54 publications

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“…We found that the DNAbinding activity of C/EBP/3 appeared in HL-60 cells after VD3treatment with little change in C/EBP/3 level. Other investigators similarly reported that DNAbinding activity of C/EBP^increased after stimulation, whereas the amount of C/EBP/3 remained unchanged, suggesting that C/EBP/3 was activated through post-translational modification (1,60). Similar post-translational modifi cation of C/EBP/3 may occur in VD3-treated HL-60 cells.…”

Section: Discussionmentioning

confidence: 73%

“…The antibody stained discrete two protein bands with molecular masses of 46 and 44 kDa; the 44 kDa band was stained much stronger by the antibody. These two proteins are considered to be derived from the first two AUGcodons of C/EBP/3 mRNA (1,60). The intensity of the two signals did not significantly change in HL-60 cells after VD3treatment (Fig.…”

Section: Expression Of Mrp14in Human Monocytic Leukemia Cellsmentioning

confidence: 99%

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Transcriptional Regulation by C/EBP.ALPHA. and -.BETA. in the Expression of the Gene for the MRP14 Myeloid Calcium Binding Protein.

Kuruto-Niwa

Nakamura

Takeishi

et al. 1998

Cell Struct. Funct.

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ABSTRACT.Transcriptional regulation of the gene for the myeloid calcium binding protein, MRP14, was investigated in humanmonocytic leukemia cell lines. The MRP14gene was not expressed in monoblastic ML-1 cells, promonocytic U-937 cells, or promyelocytic HL-60 cells. On the other hand, the gene was expressed in monocytic THP-1 cells and in the HL-60 cells treated with 1,25-dihydroxyvitamin D3 (VD3). The level of MRP14in VD3-treated HL-60 cells was two-fold higher than that in THP-1 cells. Amongseveral known transcription factor binding motifs, nuclear protein(s) of VD3-treated HL-60 cells and THP-1 cells bound to the CCAAT/enhancerbinding protein (C/EBP)-binding motif that was located in the upstream region of the MRP14gene (-81), as evidenced by the competitive gel mobility-shift assay. An antibody for C/EBPa supershifted the nucleoprotein complex in THP-1 cells but not in the VD3-treated HL-60 cells, whereas an antibody for C/EBP^blocked the formation of the complex with the nuclear factor of the HL-60 cells but not with that of THP-1 cells. An anti-C/EBPd antibody had no effect on the complex in either cell. Thus, it was concluded that C/EBPa and -fi were able to bind to the C/EBP motif, and that C/EBPa bound to the motif in THP-1 cells and C/EBP^bound to that in the VD3-treated HL-60 cells. Furthermore, to examine the transcriptional activity of the C/EBP motif, we transfected several constructed luciferase reporter DNAsinto HL-60 cells and THP-1 cells. The luciferase activity of the C/EBP motif in HL-60 cells was increased by VD3treatment. The C/EBP motif in the MRP14gene was confirmed to function as a regulatory region in VD3-treated HL-60 cells and THP-1 cells by the assay. Since C/EBP/9 was also detected in VD3-untreated HL-60 cells by immunoblotting, VD3 activated C/EBP/9 to bind to the motif, probably through post-translational modification.Myeloid calcium binding proteins, MRP8and MRP14 (25, 35), also designated cystic fibrosis antigen (5, 12), the leukocyte LI molecule (4), the 60B8 antigen (34, 55), p8/pl4 (17), calgranulin A/B (22), and calprotectin (51, 66), are members of the S100 protein family, whose genes are knownto be localized in the cluster on human chromosome Iq21 (46). Therefore, it has been proposed that MRP8and MRP14be called S100A8 and S100A9, respectively (46).

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Section: Discussionmentioning

confidence: 73%

Section: Expression Of Mrp14in Human Monocytic Leukemia Cellsmentioning

confidence: 99%

Transcriptional Regulation by C/EBP.ALPHA. and -.BETA. in the Expression of the Gene for the MRP14 Myeloid Calcium Binding Protein.

Kuruto-Niwa

Nakamura

Takeishi

et al. 1998

Cell Struct. Funct.

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“…Studies using STAT-1␣-deficient microglia and the specific NF-B inhibitor SN50 prove that STAT-1␣ and NF-B activation are required for IFN-␥-and TNF-␣-mediated Fas induction in microglia, respectively. In HeLa cells, CCAAT/enhancer-binding protein ␤ (C/ EBP␤) is responsible for influenza virus-infection mediated Fas up-regulation (44). In addition, NF-B and C/EBP consensus elements are suggested to be involved in rat Fas expression (45).…”

Section: Discussionmentioning

confidence: 99%

Differential Regulation and Function of Fas Expression on Glial Cells

Lee¹,

Zhou

Choi³

et al. 2000

The Journal of Immunology

121

104

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Fas/Apo-1 is a member of the TNF receptor superfamily that signals apoptotic cell death in susceptible target cells. Fas or Fas ligand (FasL)-deficient mice are relatively resistant to the induction of experimental allergic encephalomyelitis, implying the involvement of Fas/FasL in this disease process. We have examined the regulation and function of Fas expression in glial cells (astrocytes and microglia). Fas is constitutively expressed by primary murine microglia at a low level and significantly up-regulated by TNF-α or IFN-γ stimulation. Primary astrocytes express high constitutive levels of Fas, which are not further affected by cytokine treatment. In microglia, Fas expression is regulated at the level of mRNA expression; TNF-α and IFN-γ induced Fas mRNA by ∼20-fold. STAT-1α and NF-κB activation are involved in IFN-γ- or TNF-α-mediated Fas up-regulation in microglia, respectively. The cytokine TGF-β inhibits basal expression of Fas as well as cytokine-mediated Fas expression by microglia. Upon incubation of microglial cells with FasL-expressing cells, ∼20% of cells underwent Fas-mediated cell death, which increased to ∼60% when cells were pretreated with either TNF-α or IFN-γ. TGF-β treatment inhibited Fas-mediated cell death of TNF-α- or IFN-γ-stimulated microglial cells. In contrast, astrocytes are resistant to Fas-mediated cell death, however, ligation of Fas induces expression of the chemokines macrophage inflammatory protein-1β (MIP-1β), MIP-1α, and MIP-2. These data demonstrate that Fas transmits different signals in the two glial cell populations: a cytotoxic signal in microglia and an inflammatory signal in the astrocyte.

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“…Although the death receptor-mediated apoptosis pathway induced by influenza infection has been extensively studied Wada et al, 1995;Fujimoto et al, 1998), little is known about the potential participation of the mitochondriamediated apoptosis pathway during influenza-induced cell death. Although PK-15 cells are not commonly used for swine influenza virus replication, our results shown in Figure 1 demonstrated that PK-15 cell was shown to fully support SIV replications.…”

Section: Discussionmentioning

confidence: 99%

Activation of the intrinsic mitochondrial apoptotic pathway in swine influenza virus-mediated cell death

Choi

Kim²,

Kim³

et al. 2006

Exp Mol Med

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Transcription Stimulation of the Fas-encoding Gene by Nuclear Factor for Interleukin-6 Expression upon Influenza Virus Infection

Cited by 94 publications

References 54 publications

Transcriptional Regulation by C/EBP.ALPHA. and -.BETA. in the Expression of the Gene for the MRP14 Myeloid Calcium Binding Protein.

Transcriptional Regulation by C/EBP.ALPHA. and -.BETA. in the Expression of the Gene for the MRP14 Myeloid Calcium Binding Protein.

Differential Regulation and Function of Fas Expression on Glial Cells

Activation of the intrinsic mitochondrial apoptotic pathway in swine influenza virus-mediated cell death

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