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The study of the role of 2 kinds of TNF receptors regulating the TNF-induced apoptosis in eosinophils.

The study of the role of 2 kinds of TNF receptors regulating the TNF-induced apoptosis in eosinophils.
2种TNF受体调节TNF诱导的嗜酸性粒细胞凋亡的作用研究。
批准号:
09670466
负责人:
DOBASHI Kunio
金额:
$2.37万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 1999

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中文摘要
翻译
Apoptosis is important for the resolution of chronic eosinophilic inflammation observed in bronchial asthma.Using a human myeloblastic leukemia cell line,EoL-1,we investigated the effect of interferon-gamma(IFN-γ)on Fas-and tumor becrosis factor-α(TNF)-induced apoptosis.Both THN and anti-Fas monoclonal antibody(CH-11)induced apoptosis of EoL-1cells.Pretreatment with IFN-γenhanced the CH-11-induced apoptosis with up-regulation of Fas.However,the treatment markedly inhibited the TNF-induced apoptosis.In flow cytometric analysis,EoL-1expressed two types of tumor necrosis factor receptors(TNFR1,2)and the expression of TNFR2 but not of TNFR1was up-regulated significantly after the IFN-Γtreatment.The TNF-induced apoptosis was mimicked by a TNFR1stimulating antibody(htr-9),and was reversed by a TNFR1blocking antibody(H398)。Although the TNFR1-mediated cytotoxic signal was not affected by IFN-γpretreatment,blocking TNFR2 by a specific antagonistic antibody(utr-1…More)canceled the inhibitory effect of IFN-Γ。In conclusion,TNF-induced apoptosis was mediated preferentially by TNFR1,and the anti-apoptotic effect of IFN-γresult from up-regulated TNFR2 in EoL-1cell line.Further,we investigated the signal transduction pathway from TNFR2 in IFN-γtreated EoL-1cells.We revealed that the stimulation through TNFR2 activated the NF-kappaB by western blot analysis.Recently,we reported that the effect of Rho/ROCK signaling on cell functions.Rho/Rock signaling inhibited the myosin phosphatase and kept the phosphoryrated myosin high.ROCK inhibitor(Y-27632)relaxed the muskarinic bronchiai smooth muscle contraction。Myosin is known to regulates the morphological change and migration of cells.So,we investigated the effect of ROCK inhibitor(Y-27632)on migration of eosinophols and found that Y-27632 inhibitted the migration of eosinophils without inhibitting the Ca I D1++i D1 influx or production of active oxygen。These findings were preparing for paper。Less:Less
英文摘要
Apoptosis is important for the resolution of chronic eosinophilic inflammation observed in bronchial asthma. Using a human myeloblastic leukemia cell line, EoL-1, we investigated the effect of interferon-gamma (IFN-γ) on Fas- and tumor becrosis factor-α (TNF)-induced apoptosis. Both THN and anti-Fas monoclonal antibody (CH-11) induced apoptosis of EoL-1 cells. Pretreatment with IFN-γ enhanced the CH-11-induced apoptosis with up-regulation of Fas. However, the treatment markedly inhibited the TNF-induced apoptosis. In flow cytometric analysis, EoL-1 expressed two types of tumor necrosis factor receptors (TNFR1, 2) and the expression of TNFR2 but not of TNFR1 was up-regulated significantly after the IFN-Γ treatment. The TNF-induced apoptosis was mimicked by a TNFR1 stimulating antibody (htr-9), and was reversed by a TNFR1 blocking antibody (H398). Although the TNFR1-mediated cytotoxic signal was not affected by IFN-γ pretreatment, blocking TNFR2 by a specific antagonistic antibody (utr-1 … More ) canceled the inhibitory effect of IFN-Γ. In conclusion, TNF-induced apoptosis was mediated preferentially by TNFR1, and the anti-apoptotic effect of IFN-γ result from up-regulated TNFR2 in EoL-1 cell line. Further, we investigated the signal transduction pathway from TNFR2 in IFN-γ treated EoL-1 cells. We revealed that the stimulation through TNFR2 activated the NF-kappaB by western blot analysis.Recently, we reported that the effect of Rho/ROCK signaling on cell functions. Rho/Rock signaling inhibited the myosin phosphatase and kept the phosphoryrated myosin high. ROCK inhibitor (Y-27632) relaxed the muskarinic bronchiai smooth muscle contraction. Myosin is known to regulates the morphological change and migration of cells. So, we investigated the effect of ROCK inhibitor (Y-27632) on migration of eosinophols and found that Y-27632 inhibitted the migration of eosinophils without inhibitting the CaィイD1++ィエD1 influx or production of active oxygen. These findings were preparing for paper. Less
期刊论文(10)
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会议论文
Yoshii, K. iizuka, K. Dobashi, T. Horie, T. Harada, M. Mori, T. Nakazawa: "Relaxation of contracted rabbit tracheal and human bronchial smooth muscle by Y-27632 through inhibition of Ca2+ sensitization."Am. J. Respir. Cell Mol. Biol.. 20. 1190-1200 (1999)
Yoshii、K. iizuka、K. Dobashi、T. Horie、T. Harada、M. Mori、T. Nakazawa:“Y-27632 通过抑制 Ca2 敏化来松弛收缩的兔气管和人支气管平滑肌。”
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Horie T.,Dobashi K.et al.: "Interferon-gamma rescues TNF-alfa induced apoptosis mediated by up-regulation of TNFR2 on EoL-1 cells"Exp. Hematol.. 27. 512-519 (1999)
Horie T.、Dobashi K.等人:“干扰素-γ 可挽救 EoL-1 细胞上 TNFR2 上调介导的 TNF-α 诱导的细胞凋亡”Exp。
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通讯作者:
Takeo Horie: "Interferon-gamma rescues TNF-alfa induced apoptosis mediated by up-regulation of TNFR2 on EoL-1 cells." Exp.Hematol.(in press). (1999)
Takeo Horie:“干扰素 γ 可挽救 EoL-1 细胞上 TNFR2 上调介导的 TNF-α 诱导的细胞凋亡。”
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