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首页> 外文期刊>Cellular immunology >TGF-beta1 expression in EL4 lymphoma cells overexpressing growth hormone.
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TGF-beta1 expression in EL4 lymphoma cells overexpressing growth hormone.

机译：TGF-beta1在过表达生长激素的EL4淋巴瘤细胞中的表达。

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摘要

Our previous studies show that growth hormone overexpression (GHo) upregulates the expression of the IGF-1R and IGF-2R resulting in the protection of the EL4 lymphoma cell line from apoptosis. In this study, we report that GHo also increases TGF-beta1 protein expression measured by luciferase promoter assay, Western analysis, and ELISA. Further, the data show that antibody to TGF-betaR2 decreases TGF-beta1 promoter activity to the level of vector alone control cells. GHo cells treated with (125)I-rh-latent TGF-beta1 showed increased activation of latent TGF-beta1 as measured by an increase in the active 24kDa, TGF-beta1 compared to vector alone control cells. The ability of endogenous GH to increase TGF-beta1 expression is blocked in EL4 cells by antisense but not sense oligodeoxynucleotides or in cells cultured with antibody to growth hormone (GH). The data suggest that endogenous GH may protect from apoptosis through the IGF-1R receptor while limiting cellular growth through increased expression and activation of TGF-beta1.
机译：我们以前的研究表明，生长激素过度表达（GHo）上调了IGF-1R和IGF-2R的表达，从而保护了EL4淋巴瘤细胞系免于凋亡。在这项研究中，我们报告GHo还可以通过荧光素酶启动子测定，Western分析和ELISA来提高TGF-beta1蛋白的表达。此外，数据显示针对TGF-βR2的抗体将TGF-β1启动子活性降低至单独载体对照细胞的水平。与单独的载体对照细胞相比，用活性的24kDaTGF-β1的增加来衡量，用（125）I-rh潜在的TGF-β1处理的GHo细胞显示出潜在的TGF-β1的激活增加。内源性GH增加TGF-β1表达的能力在EL4细胞中被反义阻断，但没有感觉到寡脱氧核苷酸或在用生长激素（GH）抗体培养的细胞中被阻断。数据表明内源性GH可以通过IGF-1R受体防止细胞凋亡，同时通过增加TGF-beta1的表达和激活来限制细胞生长。

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