上海交通大学学报（医学版）

上海交通大学学报（医学版）

• 论著（临床研究） • 上一篇    下一篇

原发性醛固酮增多症患者病变肾上腺组织中PI3K/AKT/mTOR信号通路分子的表达

宿恒川，黄 欣，戴 军，周文龙，黄宝星，曹万里，孙福康   

  1. 上海交通大学 医学院附属瑞金医院泌尿外科， 上海 200025
  • 出版日期:2013-09-28 发布日期:2013-09-29
  • 通讯作者: 孙福康, 电子信箱: sunfukang6@126.com。
  • 作者简介:宿恒川(1987—)，男，硕士; 电子信箱: suhengchuan@163.com。
  • 基金资助:

    上海市自然科学基金(10411960000)

Expression of PI3K/AKT/mTOR signaling pathway in diseased adrenal glands in patients with primary aldosteronism

SU Heng-chuan, HUANG Xin, DAI Jun, ZHOU Wen-long, HUANG Bao-xing, CAO Wan-li, SUN Fu-kang   

  1. Department of Urology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China
  • Online:2013-09-28 Published:2013-09-29
  • Supported by:

    Shanghai Natural Science Foundation, 10411960000

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摘要：

目的 探讨原发性醛固酮增多症（原醛症）患者病变肾上腺组织中PI3K/AKT/mTOR信号通路分子的表达特点及意义。方法 以接受手术治疗且临床和病理学资料完整的45例原醛症患者作为研究对象，采用免疫组织化学法和Western blotting方法检测肾上腺组织中PI3K/AKT/mTOR信号通路关键蛋白p-AKT、p-mTOR、p-S6及血管内皮生长因子（VEGF）的表达情况。以肾细胞癌患者及其施行手术时切取的正常肾上腺组织作为对照组（n=12）。结果 原醛症患者表现为干渴、多尿、难治性高血压和低钾、高醛固酮及低肾素血症。与对照组比较，原醛症患者病变肾上腺组织中p-AKT、p-mTOR、p-S6及VEGF的表达明显增高(P<0.05）；原醛症患者血浆醛固酮水平和病变肾上腺组织中，p-AKT与p-mTOR的表达量呈显著正相关(r2p-AKT=0.356, P<0.01；r2p-mTOR=0.295, P<0.05)。结论 原醛症患者病变肾上腺组织中PI3K/AKT/mTOR 信号通路关键蛋白p-AKT、p-mTOR、p-S6及VEGF的表达显著增强，提示PI3K/AKT/mTOR信号通路在肾上腺原醛症的发生和发展中发挥重要作用。

关键词: 原发性醛固酮增多症, 醛固酮腺瘤, 特发性醛固酮增多症, p-AKT, p-mTOR, p-S6, 血管内皮生长因子

Abstract:

Objective To investigate the expression of PI3K/AKT/mTOR signaling pathway in the diseased adrenal glands of patients with primary aldosteronism. Methods Forty-five patients with primary aldosteronism undergoing surgical treatment with complete clinical and pathological records were selected. The expression of pAKT, p-mTOR, p-S6 and vascular endothelial growth factor (VEGF) in the tissues of diseased adrenal glands was determined by immunohistochemical staining and Western blotting. The resected normal tissues of adrenal glands in surgical treatment in patients with renal cell carcinoma were served as control group (n=12). Results Patients with primary aldosteronism presented with polydipsia, polyuria, refractory hypertension, profound hypokalemia, hyperaldosteronemia and decreased plasma renin activity. The expression of p-AKT, p-mTOR, p-S6 and VEGF in diseased adrenal glands in patients with primary aldosteronism was significantly higher than that in controls (P<0.05). The plasma aldosterone level was positively significantly related to the expression of p-AKT and p-mTOR in diseased adrenal glands in patients with primary aldosteronism (r2p-AKT=0.356, P<0.01；r2p-mTOR=0.295, P<0.05). Conclusion The expression of p-AKT, p-mTOR, p-S6 and VEGF of PI3K/AKT/mTOR signaling pathway in diseased adrenal tissues is significantly increased in patients with primary aldosteronism, which may participate in the development of primary aldosteronism.

Key words: primary aldosteronism, aldosterone-producing adenoma, bilateral idiopathic hyperaldosteronism, p-AKT, p-mTOR, p-S6, VEGF