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首页> 外文会议>Annual Meeting of the Japanese Association for Animal Cell Technology >NEGATIVE REGULATION OF THE BASOPHIL ACTIVATION BY NATURAL LIGANDS FOR PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS
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NEGATIVE REGULATION OF THE BASOPHIL ACTIVATION BY NATURAL LIGANDS FOR PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS

机译：天然配体对过氧化物体增殖物激活的受体的天然配体的阴性调节

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Peroxisome proliferator-activated receptors (PPARs) are the nuclear receptor type transcription factors, and have been shown to play an important role in regulating adipocyte differentiation and glucose homeostasis. Recently, immunoregulative functions of PPARs are gradually elucidated. Allergy is a hyperimmune response, and basophils and mast cells, which expressed the high-affinity IgE receptor FceRI on the cell surface, have a pivotal role in the IgE-mediated allergic response. To investigate a possible role of PPAR in human basophils, the effect of naturally occurring ligands for PPAR α, β, and γ on the FcsRI expression in the human basophilic KU812 cells was studied. Treatment with Prostaglandin (PG) A_1 or 15-deoxy-Δ~(12, 14) PGJ_2 (15d-PGJ_2), ligands for PPARp or PPARy, respectively, was shown to be able to suppress the cell surface expression of FcsRI. In order to reveal whether the reduction of FceRI expression by PPAR ligands is associated with a functional change, histamine releasefrom KU812 cells in response to cross-linkage of FceRI was examined. Both PPAR ligands inhibited the histamine release from KU812 cells due to the lack of FceRI available to cross-link. Moreover, RT-PCR analysis showed that KU812 cells expressed the mRNAfor PPAR α, β, and γ, implicating that PPAR β or γ may be related to negative regulation of the cell activation via FcεRI. In addition, PGA, or 15d-PGJ_2 treatment decreased the mRNA of a and/or γ subunit of FcεRI, implicating that suppressive effect of FcεRI by PPARs may be due to the down-regulation of FcεRI α and/or y mRNA.
机译：过氧化物体增殖剂活化受体（PPAR）是核受体类型转录因子，并且已被证明在调节脂肪细胞分化和葡萄糖稳态方面发挥重要作用。最近，PPAR的免疫抑制功能逐渐阐明。过敏是一种超敏反应，嗜碱性粒细胞和肥大细胞，其在细胞表面上表达高亲和力IgE受体Fceri，在IgE介导的过敏反应中具有枢转作用。为了研究PPAR在人嗜碱性浴中的可能作用，研究了对PPARα，β和γ对人嗜碱性Ku812细胞中FCSRI表达上的天然存在的配体对PPARα，β和γ的影响。分别用前列腺素（PG）A_1或15-脱氧-δ〜（12,14）PGJ_2（15d-PGJ_2），分别用于PPAPLP或PPARA的pGJ_2（15d-PGJ_2），抑制FCSRI的细胞表面表达。为了揭示PPAR配体的Fceri表达是否与官能变化有关，检查了响应于Fceri的交联的组胺氟脲酰库ku812细胞。由于缺乏可用于交联的Fceri，PPAR配体均抑制来自Ku812细胞的组胺释放。此外，RT-PCR分析表明Ku812细胞表达MRNAFORPPARα，β和γ，这意味着PPARβ或γ可以与通过FCεRI对细胞活化的负调节有关。此外，PGA或15d-PGJ_2处理降低了FcεRi的A和/或γ亚基的mRNA，这意味着FcεRi通过PPAR的抑制作用可能是由于FCεRIα和/或Y mRNA的下调。

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