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首页> 外文期刊>Life sciences >Activation of protein kinase B/Akt by alpha1-adrenoceptors in the human prostate
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Activation of protein kinase B/Akt by alpha1-adrenoceptors in the human prostate

机译：人前列腺中α1-肾上腺素受体对蛋白激酶B / Akt的激活

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Aims: Besides their role in contraction, α1-adrenoceptors may be involved in prostate hyperplasia. This would require receptor signaling by growth-promoting pathways. Akt (syn. Protein kinase B) is an important regulator of growth and differentiation. Objective: To investigate whether α1-adrenoceptors in the human prostate activate Akt. Main methods: Prostate tissue was obtained from patients undergoing radical prostatectomy. Akt expression was investigated by RT-PCR, Western blot, and immunohistochemistry. Akt activation by noradrenaline (30 μM) and phenylephrine (10 μM) was assessed by Western blot analyses with a phospho-specific antibody. The effects of the Akt inhibitors FPA-124 and 10-DEBC on phenylephrine-, noradrenaline- and electric field stimulation- (EFS-) induced contraction were studied in myographic measurements. Key findings: mRNA of all three Akt isoforms (Akt1, Akt2, Akt3) was detected by RT-PCR in all prostate samples (n = 6 patients). Protein expression was confirmed by Western blot analysis (n = 8 patients). Immunohistochemical staining for Akt revealed strong immunoreactivity in prostate smooth muscle cells (n = 5 patients). Stimulation of prostate tissues with noradrenaline (30 μM, n = 8 patients) or phenylephrine (10 μM, n = 7 patients) caused significant Akt phosphorylation at serine-473, indicating activation of Akt. FPA124 and 10-DEBC were without effects on noradrenaline-, phenylephrine-, or EFS-induced contraction of prostate strips. Significance: Prostate α1-adrenoceptors activate Akt. Consequently, Akt is a target of α1-blocker therapy, which has been unknown to date. Our findings point to functions of prostate α1-adrenoceptors besides contraction.
机译：目的：α1-肾上腺素受体除了在收缩中发挥作用外，还可能参与前列腺增生。这将需要通过促生长途径的受体信号传导。 Akt（蛋白激酶B的合成）是生长和分化的重要调节剂。目的：研究人前列腺中的α1-肾上腺素受体是否激活Akt。主要方法：前列腺组织取自接受前列腺根治术的患者。通过RT-PCR，蛋白质印迹和免疫组化研究Akt表达。用磷酸特异性抗体通过蛋白质印迹分析评估去甲肾上腺素（30μM）和去氧肾上腺素（10μM）的Akt激活。在肌电图测量中研究了Akt抑制剂FPA-124和10-DEBC对去氧肾上腺素，去甲肾上腺素和电场刺激（EFS）引起的收缩的影响。关键发现：通过RT-PCR在所有前列腺样品（n = 6例患者）中检测到所有三种Akt亚型（Akt1，Akt2，Akt3）的mRNA。蛋白表达通过蛋白质印迹分析证实（n = 8例患者）。 Akt的免疫组织化学染色显示前列腺平滑肌细胞中有很强的免疫反应性（n = 5例）。用去甲肾上腺素（30μM，n = 8例患者）或去氧肾上腺素（10μM，n = 7例）刺激前列腺组织会导致丝氨酸473处的Akt磷酸化显着，表明Akt的激活。 FPA124和10-DEBC对去甲肾上腺素，去氧肾上腺素或EFS引起的前列腺带收缩没有影响。意义：前列腺α1-肾上腺素能激活Akt。因此，Akt是α1受体阻滞剂治疗的靶标，迄今为止尚不清楚。我们的研究结果指出了前列腺α1-肾上腺素受体除了收缩功能。

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