Synergistic effects of estradiol and 11-ketotestosterone on vitellogenin physiology in the shortfinned eel (Anguilla australis)
Synergistic effects of estradiol and 11-ketotestosterone on vitellogenin physiology in the shortfinned eel (Anguilla australis)
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雌二醇和 11-酮睾酮对短鳍鳗（Anguilla australis）卵黄蛋白原生理学的协同作用
DOI：
10.1093/biolre/ioz007
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发表时间：
2019
影响因子：
3.6
通讯作者：
P Mark Lokman
中科院分区：
文献类型：
--
作者：
Thomson-Laing Georgia;Erin L Damsteegt;Jun Nagata;Shigeho Ijiri;Shinji Adachi;Takashi Todo;Naoshi Hiramatsu;P Mark Lokman
雌激素17β（E2）和11-酮睾酮（11 KT）分别参与卵黄发生和卵泡刺激素受体（fshr）的调节。为了克服捕获诱导的生殖阻滞在短鳍鳗，南极，我们假设，在组合中，11 KT和E2将刺激卵巢卵黄蛋白原（Vtg）的摄取。早期青春期鳗鱼接受激素植入剂含有不同浓度的E2（0，0.2，2，5毫克）与或不与11 KT（1毫克）。通过组织学检查、qPCR、免疫印迹或单向放射免疫扩散测定血浆、肝脏和卵巢组织中的Vtg水平。分别分析垂体和卵巢中促性腺激素β亚基和促性腺激素受体的表达，以确定类固醇作用的机制。当单独给药时，E2增加肝脏产生和血浆Vtg水平。相反，11 KT降低血浆Vtg水平，似乎减少其生产。11 KT和E2均不能诱导卵母细胞摄取Vtg，但E2处理对Vtg的摄取是必需的。尽管11 KT显著增加了卵母细胞的大小和fshrmRNA水平，但情况仍然如此。令人惊讶的是，11 KT和E2的共同处理成功地诱导了Vtg的摄取，这表明11 KT可能有助于Vtg掺入发育中的卵母细胞。这些结果突出了潜在的性类固醇共治疗，一种方法，旨在模仿野生鳗鱼卵子发生，诱导卵黄发生，特别是卵巢卵黄沉积，即使在没有外源性促性腺激素治疗。
Estradiol-17β (E2) and 11-ketotestosterone (11KT) have been implicated in vitellogenesis and in regulating expression of the follicle-stimulating hormone receptor (fshr), respectively. To override the captivity-induced reproductive block in shortfinned eel,Anguilla australis, we hypothesized that in combination, 11KT and E2would stimulate ovarian uptake of vitellogenin (Vtg). Early pubertal eels received hormone implants containing varying concentrations of E2(0, 0.2, 2, 5 mg) with or without 11KT (1 mg). Vtg levels were determined in plasma, liver, and ovarian tissues by histological examination, qPCR, immunoblotting, or single radial immunodiffusion. The expression of gonadotropin-beta subunits and gonadotropin receptors in the pituitary and ovary, respectively, were analyzed to determine mechanisms by which steroid effects may be exerted. When administered alone, E2increased hepatic production and plasma levels of Vtg. In contrast, 11KT decreased plasma levels of Vtg, seemingly reducing its production. Neither 11KT nor E2could induce uptake of Vtg into oocytes, although E2treatment appeared necessary for uptake to occur. This was the case despite 11KT dramatically increasing both oocyte size andfshrmRNA levels. Astonishingly, the uptake of Vtg was successfully induced by co-treatment with 11KT and E2, suggesting that 11KT might facilitate the incorporation of Vtg into the developing oocyte. These results highlight the potential of sex steroid co-treatment, an approach aimed at mimicking oogenesis in wild eels, to induce vitellogenesis, specifically ovarian yolk deposition, even in the absence of exogenous gonadotropin treatment.