University of California, Davis, USA.
Anim Reprod Sci. 2012 Nov;135(1-4):106-12. doi: 10.1016/j.anireprosci.2012.09.003. Epub 2012 Sep 20.
Reducing prepubertal endogenous estrogens led to increased numbers of Sertoli cells and the associated increased testicular size and testicular sperm production capacity in boars. The increased number of Sertoli cells might be due to a longer time for proliferation; delayed differentiation of Sertoli cells during suppressed endogenous estrogens would be consistent with this hypothesized, prolonged proliferation interval. This study used immunohistochemical detection of anti-Müllerian hormone (AMH), a marker of immature Sertoli cells, and of CDKN1B, a cell cycle inhibitor associated with more mature Sertoli cells, to determine if suppressing endogenous estrogens detectably delayed "differentiation" of porcine Sertoli cells. Testes were from littermate pairs of boars previously treated with Letrozole, an aromatase inhibitor, or vehicle, from the first week of age until tissue collection at 2, 3, 4, 5 or 6 months of age. Four animals were examined at each age following Letrozole treatment and their corresponding littermates evaluated following treatment with vehicle. Amount of AMH protein in Sertoli cells decreased with age of boar and could not be detected at 6 months of age. The AMH labeling was greater in the Letrozole-treated boars compared with littermate vehicle controls at 4 months of age (P=0.03). The percentage of CDKN1B-labeled Sertoli cells apparently increased with age through 5 months of age. At 4 and 5 months of age, the mean percentage of CDKN1B-labeled Sertoli cells was less in the Letrozole-treated animals than in the vehicle control animals (P = 0.03 and 0.04, respectively). These results are consistent with the hypothesis that continual inhibition of aromatase (and concomitatant reduced estrogen synthesis) causes a delay in Sertoli cell maturation in boars.
降低青春期前的内源性雌激素会导致公猪的支持细胞数量增加，进而导致睾丸体积增大和睾丸精子生成能力增强。支持细胞数量的增加可能是由于增殖时间延长所致；在抑制内源性雌激素期间，支持细胞的分化延迟，这与假设的增殖间隔延长是一致的。本研究使用抗苗勒管激素（AMH）的免疫组织化学检测，AMH 是未成熟支持细胞的标志物，以及细胞周期抑制剂 CDKN1B，来确定抑制内源性雌激素是否可检测到延迟猪支持细胞的“分化”。睾丸来自先前用芳香酶抑制剂来曲唑或载体处理的公猪的同窝对，从出生后的第一周开始，直到 2、3、4、5 或 6 个月时收集组织。在来曲唑处理后，每个年龄组检查 4 只动物，并在处理后评估其相应的同窝对照。随着公猪年龄的增长，支持细胞中的 AMH 蛋白含量减少，6 个月时无法检测到。与同窝对照的载体处理动物相比，来曲唑处理的公猪在 4 个月时 AMH 标记更高（P=0.03）。通过 5 个月龄，CDKN1B 标记的支持细胞的百分比显然随着年龄的增长而增加。在 4 个月和 5 个月龄时，来曲唑处理的动物中 CDKN1B 标记的支持细胞的平均百分比明显低于载体对照动物（分别为 P=0.03 和 0.04）。这些结果与持续抑制芳香酶（并伴随雌激素合成减少）导致公猪支持细胞成熟延迟的假设一致。
