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17-β-雌二醇促进部分胰腺切除小鼠模型中的胰岛细胞增殖。

17-Estradiol Promotes Islet Cell Proliferation in a Partial Pancreatectomy Mouse Model.

作者信息

Wu Tingting, Xu Jinyong, Xu Shengchun, Wu Lianzhong, Zhu Youyu, Li Guangwu, Ren Zhenhua

机构信息

Department of Neurobiology, School of Basic Medicine, Anhui Medical University, Hefei, Anhui 230032, China.

Department of Anatomy, School of Basic Medicine, Anhui Medical University, Hefei, Anhui 230032, China.

出版信息

J Endocr Soc. 2017 Jun 5;1(7):965-979. doi: 10.1210/js.2016-1073. eCollection 2017 Jul 1.

DOI:10.1210/js.2016-1073
PMID:29264547
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5686603/
Abstract

17-Estradiol (E2) is a multifunctional steroid hormone in modulating metabolism . Previous studies have reported that E2 could promote insulin secretion and protect cells from apoptosis. In this study, the partial pancreatectomy (PPx) model was used to study the role of E2 in islet cell proliferation. The animals were divided into four groups, including sham control, PPx model, E2, and E2 plus estrogen antagonist (E2 plus ICI) groups. In the E2 group, 5-bromo-2'-deoxyuridine- and Ki67-positive cells significantly increased after PPx, and the protein expression of forkhead transcription factor M1, cyclin A2, cyclin B1, and cyclin E2 also significantly increased in the isolated islets. The messenger RNA expression of cyclin A2 and cyclin B2 increased in E2 treatment group. Additionally, the effects of E2 on the PPx mice were partially blocked by estrogen antagonist ICI182,780. The results indicated that E2 significantly promoted islet cell proliferation in PPx model mice, and it upregulated the expression of cell cycle genes. In conclusion, E2 treatment is beneficial for islet cell proliferation in adult mice after PPx. A partial pancreatectomy in mice may be an attractive model for the study of islet cell proliferation.

摘要

17-β-雌二醇(E2)是一种调节代谢的多功能甾体激素。先前的研究报道,E2可促进胰岛素分泌并保护细胞免于凋亡。在本研究中,采用部分胰腺切除术(PPx)模型来研究E2在胰岛细胞增殖中的作用。动物被分为四组,包括假手术对照组、PPx模型组、E2组以及E2加雌激素拮抗剂组(E2加ICI组)。在E2组中,PPx术后5-溴-2'-脱氧尿苷和Ki67阳性细胞显著增加,并且分离的胰岛中叉头转录因子M1、细胞周期蛋白A2、细胞周期蛋白B1和细胞周期蛋白E2的蛋白表达也显著增加。细胞周期蛋白A2和细胞周期蛋白B2的信使核糖核酸表达在E2治疗组中增加。此外,雌激素拮抗剂ICI182,780部分阻断了E2对PPx小鼠的作用。结果表明,E2显著促进PPx模型小鼠的胰岛细胞增殖,并上调细胞周期基因的表达。总之,E2治疗有利于成年小鼠PPx术后的胰岛细胞增殖。小鼠部分胰腺切除术可能是研究胰岛细胞增殖的一个有吸引力的模型。

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本文引用的文献

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Update on RAAS Modulation for the Treatment of Diabetic Cardiovascular Disease.糖尿病心血管疾病治疗中 RAAS 调节的最新进展。
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Worldwide trends in diabetes since 1980: a pooled analysis of 751 population-based studies with 4.4 million participants.1980年以来全球糖尿病趋势:对751项基于人群的研究进行的汇总分析,涉及440万参与者。
Lancet. 2016 Apr 9;387(10027):1513-1530. doi: 10.1016/S0140-6736(16)00618-8. Epub 2016 Apr 6.
8
mTORC1 pathway mediates beta cell compensatory proliferation in 60 % partial-pancreatectomy mice.mTORC1信号通路介导60%胰腺部分切除术小鼠的β细胞代偿性增殖。
Endocrine. 2016 Jul;53(1):117-28. doi: 10.1007/s12020-016-0861-5. Epub 2016 Jan 27.
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Insulin demand regulates β cell number via the unfolded protein response.胰岛素需求通过未折叠蛋白反应调节β细胞数量。
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10
Estrogen Receptor α Regulates β-Cell Formation During Pancreas Development and Following Injury.雌激素受体α在胰腺发育及损伤后调节β细胞形成。
Diabetes. 2015 Sep;64(9):3218-28. doi: 10.2337/db14-1798. Epub 2015 May 26.