Molecular characterization of five steroid receptors from pengze crucian carp and their expression profiles of juveniles in response to 17 alpha-ethinylestradiol and 17 alpha-methyltestosterone

文献类型: 外文期刊

第一作者: Zheng, Yao

作者: Zheng, Yao;Li, Meng;Qin, Fang;Liu, Shaozhen;Wang, Houpeng;Wu, Tingting;Zhang, Yingying;Wang, Zaizhao;Wang, Lihong;Liang, Hongwei

作者机构:

关键词: 17 alpha-Ethinylestradiol;17 alpha-Methyltestosterone;Juvenile pengze crucian carp;Estrogen receptor;Androgen receptor;Vitellogenin

期刊名称:GENERAL AND COMPARATIVE ENDOCRINOLOGY ( 影响因子:2.822; 五年影响因子:2.772 )

ISSN: 0016-6480

年卷期: 2013 年 191 卷

页码:

收录情况: SCI

摘要: Pengze crucian carp (Carassius auratus var. pengze, Pcc), a triploid gynogenetic fish, was used in this study to investigate the cross-talk between EDCs and steroid receptors. The full-length cDNAs of five steroid receptors (esr1, er alpha2, esr2a, esr2b, ar) and partial cDNA of vtg B were isolated. The tissue distributions of these genes were analyzed in adult fish by qRT-PCR. Then the expression profiles of five steroid receptors (esrs and ar) and vtg B were detected in the juveniles exposed to 17 alpha-ethinylestradiol (EE2, 0.1, 1 and 10 ng/L) and 17 alpha-methyltestosterone (MT, 50 mu g/L) for 4 weeks. The results demonstrated that esrs, ar, and vtg B were predominantly expressed in liver of adult fish. However, among these detected genes, esr1 and er alpha2 mRNAs are sensitive biomarkers in response to EE2 at 0.1, 1, and 10 ng/L for 1 and 2 weeks compared to esr2a, esr2b, ar, and vtg B in the juveniles of mono-female gynogenetic fish. Totally, the subtypes of esrs show biphasic responses to EE2 exposures for 4 weeks, and most of the EE2 exposures at 0.1, 1, and 10 ng/L for 1, 2, 3 and 4 weeks did not induce the mRNA expressions of vtg B. However, 1-, 2-, and 4-week 50 mu g/L MT all significantly stimulated vtg B transcripts. Further investigations are needed to elucidate the mechanism underlying the insensitivity or down-regulation of vtg B mRNA in response to EE2 in juvenile Pcc. (C) 2013 Elsevier Inc. All rights reserved.

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