Thyroid hormone modulates androgen and oestrogen receptor content in the Sertoli cells of peripubertal rats.
Thyroid hormone modulates androgen and oestrogen receptor content in the Sertoli cells of peripubertal rats.
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DOI：
10.1677/joe.0.1480043
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发表时间：
1996
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影响因子：
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通讯作者：
M. L. Panno;D. Sisci;M. Salerno;M. Lanzino;V. Pezzi;E. G. Morrone;L. Mauro;S. Palmero;E. Fugassa;S. Andò
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文献类型：
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作者：
M. L. Panno;D. Sisci;M. Salerno;M. Lanzino;V. Pezzi;E. G. Morrone;L. Mauro;S. Palmero;E. Fugassa;S. Andò
三碘甲状腺原氨酸（T3）对睾丸类固醇和支持细胞之间的相互作用的可能作用已被研究的基础上，以前的研究结果表明，芳香化酶活性和雌二醇的生产在青春期前后的支持细胞的T3的直接抑制作用。在这种情况下，本研究的重点是T3的影响，雌激素受体（ER）和雄激素受体（AR）的内容在细胞质和细胞核的支持细胞分离2-，3-和4周龄甲状腺功能正常，甲状腺功能减退和甲状腺功能减退治疗的大鼠。从出生到2、3、4周龄处死大鼠，用0.025%他巴唑（MMI）灌胃诱发甲状腺功能减退。在死亡前的最后一周，对一半MMI处理的动物腹膜内注射L-三碘甲状腺原氨酸（T3; 3微克/100 g体重）。来自所有组的支持细胞最初在基础条件下培养前24小时，随后在睾酮存在下（有或没有T3）再培养24小时。甲状腺功能减退症与身体和睾丸生长严重受损有关。正常甲状腺ER显示Kd升高（0.76 nM），这在研究的不同年龄组中相似。在体外添加T3或睾酮诱导ER含量的减少，这种减少是更大的暴露后，这两种激素。在2和3周龄甲状腺功能减退大鼠，ER含量显着增加，并在甲状腺功能正常大鼠逆转时，T3在体内。当ER在2和3周龄动物的支持细胞核和细胞质中进行测定时，观察到两个细胞室中ER含量的强烈关系。测试的激素似乎都没有显着影响细胞核中的AR含量，而在体外添加睾酮或T3或两种激素一起增强了AR在胞质溶胶中的更大程度上，导致其总（胞质和核）含量在细胞中的增加。目前的数据表明，T3下调雌激素受体和上调AR在青春期支持细胞。睾酮和T3在上调AR中的累加效应可能涉及T3在影响精子发生过程中支持细胞的雄激素反应性中的作用。
A possible role of tri-iodothyronine (T3) on the interplay between testicular steroids and Sertoli cells has been investigated on the basis of previous findings demonstrating a direct inhibitory influence of T3 on aromatase activity and oestradiol production in peripuberal Sertoli cells. In this context, the present study was focused on the effects of T3 on oestrogen receptor (ER) and androgen receptor (AR) contents in the cytosol and nucleus of Sertoli cells isolated from 2-, 3- and 4-week-old euthyroid, hypothyroid and hypothyroid treated rats. Hypothyroidism was induced by the oral administration of 0.025% methimazole (MMI) from birth until the rats were killed at 2, 3 and 4 weeks of age. Half of the MMI-treated animals were injected i.p. with L-tri-iodothyronine (T3; 3 micrograms/100 g body weight) during the last week before death. Sertoli cells from all groups were initially cultured under basal conditions for the first 24 h and subsequently in the presence of testosterone with or without T3 for an additional 24 h. Hypothyroidism was associated with severe impairment of body as well as testicular growth. Euthyroid ERs showed an elevated Kd (0.76 nM) which was similar in the different age groups investigated. The in vitro addition of T3 or testosterone induced a decrease in ER content and this decrease was greater after exposure to both hormones. In 2- and 3-week-old hypothyroid rats, ER content was markedly increased and was reversed in euthyroid rats when T3 was given in vivo. When ERs were assayed in the Sertoli cell nucleus and cytoplasm of 2- and 3-week-old animals, a strong relationship in ER content in the two cellular compartments was observed. Neither of the hormones tested seemed to affect the AR content in the nucleus significantly, while the in vitro addition of testosterone or T3 or both hormones together augmented the ARs in the cytosol to a greater extent, resulting in an increase in their total (cytosolic and nuclear) content in the cells. The present data suggest that T3 down-regulates ERs and up-regulates ARs in peripuberal Sertoli cells. The additive effect of testosterone and T3 in up-regulating ARs could possibly involve a role for T3 in influencing the androgen responsiveness of the Sertoli cells during spermatogenesis.