Oliveira Cleida A, Carnes Kay, França Luiz R, Hermo Louis, Hess Rex A
Department of Veterinary Biosciences, University of Illinois, 2001 S. Lincoln, Urbana, IL 61802-6199, USA.
Biol Cell. 2005 Jun;97(6):385-95. doi: 10.1042/BC20040078.
Efferent ductules reabsorb more than 90% of the rete testis fluid, a process that involves ion transporters and AQP (aquaporin) water channels. Oestrogen has been shown to modulate the expression of the ion transporters involved in this activity, but reports of AQP regulation in the male tract have been confounding. To understand better the regulation of AQP1 and AQP9, we investigated their expression in rat efferent ductules and initial segment of the epididymis after treatment with the pure antioestrogen ICI 182,780 or bilateral efferent duct ligation, or castration, followed by hormone replacement.
Results show that AQP9 is modulated by oestrogen in the efferent ductule epithelium, but not in the initial segment of the epididymis. DHT (5alpha-dihydrotestosterone) also modulated AQP9 in efferent ductules. AQP9 was down-regulated by the antioestrogen in efferent ductules on day 45 post-treatment, which occurred before the non-ciliated cells had shown significant loss of microvilli. DHT, but not oestradiol, modulated AQP9 expression in the initial segment of the epididymis. In contrast, testosterone, DHT, oestrogen or the antioestrogen did not alter AQP1 staining, indicating constitutive expression of AQP1 in the efferent ductule epithelium. AQP1 expression was induced in peritubular cells of efferent ductules and in the initial segment of the epididymis after castration and long-term treatment with the antioestrogen. Although peritubular AQP1 staining in efferent ductules was partially reversed by the androgens, it was not reversed after any treatment in the initial segment of the epididymis.
These results demonstrate that efferent ductules are unique in requiring both oestrogen and androgen to regulate an important mediator of fluid reabsorption, whereas the initial segment is dependent only on androgen stimulation.
输出小管重吸收超过90%的睾丸网液，这一过程涉及离子转运体和水通道蛋白（AQP）水通道。雌激素已被证明可调节参与此活动的离子转运体的表达，但关于雄性生殖道中AQP调节的报道一直存在混淆。为了更好地理解AQP1和AQP9的调节机制，我们研究了用纯抗雌激素ICI 182,780处理、双侧输出小管结扎或去势后激素替代处理的大鼠输出小管和附睾起始段中它们的表达情况。
结果表明，雌激素可调节输出小管上皮中的AQP9，但对附睾起始段无此作用。双氢睾酮（DHT）也可调节输出小管中的AQP9。抗雌激素在处理后第45天使输出小管中的AQP9下调，这发生在非纤毛细胞微绒毛显著丢失之前。DHT而非雌二醇可调节附睾起始段中AQP9的表达。相比之下，睾酮、DHT、雌激素或抗雌激素均未改变AQP1的染色，表明AQP1在输出小管上皮中组成性表达。去势和长期用抗雌激素处理后，输出小管的周细胞和附睾起始段中诱导了AQP1的表达。虽然雄激素可部分逆转输出小管周细胞中AQP1的染色，但在附睾起始段，任何处理后均未逆转。
这些结果表明，输出小管在需要雌激素和雄激素共同调节液体重吸收的重要介质方面具有独特性，而附睾起始段仅依赖雄激素刺激。
