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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Enhanced expression of adipocyte-type fatty acid binding protein in murine lymphocytes in response to dexamethasone treatment.
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Enhanced expression of adipocyte-type fatty acid binding protein in murine lymphocytes in response to dexamethasone treatment.

机译:响应地塞米松治疗,鼠淋巴细胞中脂肪细胞型脂肪酸结合蛋白的表达增强。

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Fatty acids have a great influence on the process of lymphocyte apoptosis which is considered as a modulating factor of immune response in both humans and animals. However the mechanism underlying the function of fatty acids in the process of lymphocyte apoptosis is not fully understood. In this study we show that the appearance of adipocyte-type fatty acid binding protein (A-FABP) is induced upon administration of dexamethasone (DEX) in both in vivo and cultured lymphocytes, and its distinct nuclear localization occurs in close relation to the DEX-induced apoptosis process. In immunohistochemistry of mouse spleen, A-FABP-immunoreactivity starts to occur 3 h after DEX stimulation, and it massively localizes in the nucleus 8 h after the treatment, while no A-FABP-immunoreactivity is discerned in the lymphocytes of normal as well as 24 h post-injection spleen. In the murine T-cell leukemia CTLL-2 cells, A-FABP-immunoreactivity is also induced in both of the cytoplasm and nucleus when the apoptosis is induced by IL-2 retrieval together with DEX treatment, while in the presence of IL-2 A-FABP-immunoreactivity is confined to the cytoplasm with DEX treatment. On the other hand, A-FABP-immunoreactivity is not detected by IL-2 retrieval alone. The present findings altogether suggest that A-FABP and its ligands, fatty acids, play an important role in the process of apoptosis and the immune modulation induced by DEX.
机译:脂肪酸对淋巴细胞凋亡过程有很大影响,而淋巴细胞凋亡被认为是人类和动物免疫应答的调节因子。然而,脂肪酸在淋巴细胞凋亡过程中的功能机制尚不完全清楚。在这项研究中,我们表明,在体内和培养的淋巴细胞中都给予地塞米松(DEX)后,可诱导脂肪细胞型脂肪酸结合蛋白(A-FABP)的出现,并且其独特的核定位与DEX密切相关诱导的凋亡过程。在小鼠脾脏的免疫组织化学中,DEX刺激后3小时开始出现A-FABP免疫反应,并且在治疗8小时后大量出现在细胞核中,而正常淋巴细胞和正常淋巴细胞均未发现A-FABP免疫反应。注射后24小时脾脏。在小鼠T细胞白血病CTLL-2细胞中,当IL-2结合DEX处理诱导细胞凋亡时,在存在IL-2的情况下,还可以在细胞质和细胞核中诱导A-FABP免疫反应。用DEX处理将A-FABP免疫反应性限制在细胞质中。另一方面,仅通过IL-2检索不能检测出A-FABP免疫反应性。本发现完全表明,A-FABP及其配体脂肪酸在DEX诱导的细胞凋亡和免疫调节过程中起重要作用。

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