Induction of three vitellogenins by 17beta-estradiol with concurrent inhibition of the growth hormone-insulin-like growth factor 1 axis in a euryhaline teleost, the tilapia (Oreochromis mossambicus)
Induction of three vitellogenins by 17beta-estradiol with concurrent inhibition of the growth hormone-insulin-like growth factor 1 axis in a euryhaline teleost, the tilapia (Oreochromis mossambicus)
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DOI：
10.1095/biolreprod.107.060947
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发表时间：
2007-10-01
影响因子：
3.6
通讯作者：
Grau, Gordon
中科院分区：
文献类型：
--
作者：
Davis, Lori K.;Hiramatsu, Naoshi;Grau, Gordon
本研究的目的是利用雄性莫桑比克罗非鱼（Oreochromis mossambicus）作为模型来研究介导雌性硬骨鱼和一般脊椎动物体细胞和性腺生长之间生理转变的分子机制。编码多种形式的卵黄蛋白原 (Vtg)（卵黄蛋白的主要前体）的部分 cDNA 从经过雌激素处理的雄性体内克隆出来，用于开发实时定量 RT-PCR 测定，并通过血浆中 Vtg 免疫反应性测定进行补充。对从 vtg cDNA 推导的氨基酸序列进行比对分析，揭示了三种不同的罗非鱼 Vtgs，它们被分类为 Aa 型、Ab 型和 C 型 Vtgs。雄性罗非鱼单次注射5μg/g体重的17β-雌二醇(E-2)，在1天内显着增加了所有三种vtg转录物的血浆E-2和肝脏水平。 3天后血浆E-2水平下降，而血浆Vtg免疫反应性和三种vtg转录物的肝脏水平继续增加。注射 E-2 后第 1 天，雌激素受体 (esr) I 基因（而非 esr2 基因）的肝脏表达也显着增加，并在 5 天内保持升高状态。虽然血浆生长激素 (Gh) 水平不受影响，但编码 Gh 受体和胰岛素样生长因子 I (Igf1) 的转录物的肝脏表达被 E-2 抑制，血浆 Igf1 水平也是如此。这些结果清楚地表明，在涉及性腺和体细胞生长过程能量利用控制的关键肝脏调节途径的分子水平上，生长轴和生殖轴之间存在明显的负相互作用。
The objective of the present study was to utilize the male Mozambique tilapia (Oreochromis mossambicus) as a model for examining the molecular mechanisms that mediate the physiological transition between somatic and gonadal growth in female teleost fish, and in vertebrates in general. Partial cDNAs that encode multiple forms of vitellogenin (Vtg), which is the major precursor of yolk proteins, were cloned from estrogen-treated males and utilized to develop real-time quantitative RT-PCR assays, which were supplemented by an assay for Vtg immunoreactivity in the plasma. Alignment analyses of the amino acid sequences deduced from the vtg cDNAs revealed three distinct tilapia Vtgs, which were categorized as Aa-, Ab-, and C-type Vtgs. A single injection of male tilapias with 17beta-estradiol (E-2) at 5 mu g/g body weight significantly increased the plasma E-2 and hepatic levels of all three vtg transcripts within I day. Plasma E-2 levels declined after 3 days, whereas the plasma Vtg immunoreactivity and hepatic levels of the three vtg transcripts continued to increase. Hepatic expression of the estrogen receptor (esr) I gene, but not the esr2 gene, also increased markedly I day after E-2 injection and remained elevated for 5 days. While plasma growth hormone (Gh) levels were unaffected, hepatic expression of transcripts that encoded the Gh receptor and insulin-like growth factor I (Igf1) was suppressed by E-2, as were the plasma Igf1 levels. These results clearly suggest a distinct negative interplay between the growth and reproductive axes at the molecular level of key hepatic regulatory pathways involved in the control of energy utilization by gonadal and somatic growth processes.