Boujrad N, Hochereau-de Reviers M T, Carreau S
Laboratorie de Biochimie, EP CNRS 009, Université de Caen, France.
Biol Reprod. 1995 Dec;53(6):1345-52. doi: 10.1095/biolreprod53.6.1345.
In order to clarify the role of germ cells in the regulation of Sertoli cell secretions, three experimental models of germ cell depletion were used: hypodactyl rat mutation (testis weight [TW]: 55% less than controls), in utero busulfan treatment (TW: 88% less than controls), and neonatal experimental cryptorchidism (TW: 72% less than controls). The aim of this work was to compare the numbers of Leydig and Sertoli cells and the production of germ cells in each experimental model to the in vitro secretions of Leydig and Sertoli cells in conditioned media and to the hormonal serum profiles of the same animal in vivo. In the three models, serum levels of hypophyseal and testosterone hormones were significantly increased and decreased, respectively. In the absence of germ cells, the total length of seminiferous tubules, the total numbers of Sertoli and Leydig cells, and the daily production of germ cells were significantly diminished. The addition of both control and damaged seminiferous tubule culture media (STM: media conditioned by 10 cm of seminiferous tubules) to 10(6) control or damaged Leydig cells led to a further increase of testosterone production after ovine LH stimulation. However, expressed per Sertoli cell, testosterone production by control Leydig cells was reduced by addition of damaged STM as compared to addition of control STM, and similarly, the addition of control STM to damaged Leydig cells enhanced testosterone production more than did the addition of damaged STM. Secretions of transferrin per Sertoli cell in STM were reduced as compared to controls by the absence of germ cells but to a lesser extent than was production of spermatocytes and of spermatids. In conclusion, secretions by Sertoli cells of the paracrine factor involved in the control of testosterone production by Leydig cells and of transferrin are modified by germ cells.
为了阐明生殖细胞在支持细胞分泌调节中的作用,使用了三种生殖细胞耗竭的实验模型:短指大鼠突变(睾丸重量[TW]:比对照组少55%)、宫内白消安处理(TW:比对照组少88%)和新生儿实验性隐睾(TW:比对照组少72%)。这项工作的目的是将每个实验模型中的睾丸间质细胞和支持细胞数量、生殖细胞产量与条件培养基中睾丸间质细胞和支持细胞的体外分泌以及同一动物体内的激素血清谱进行比较。在这三种模型中,垂体激素和睾酮激素的血清水平分别显著升高和降低。在没有生殖细胞的情况下,生精小管的总长度、支持细胞和睾丸间质细胞的总数以及生殖细胞的每日产量均显著减少。将对照和受损生精小管培养基(STM:由10厘米生精小管条件培养的培养基)添加到10⁶个对照或受损睾丸间质细胞中,在绵羊促黄体生成素刺激后导致睾酮产量进一步增加。然而,按每个支持细胞计算,与添加对照STM相比,添加受损STM会使对照睾丸间质细胞的睾酮产量降低,同样,将对照STM添加到受损睾丸间质细胞中比添加受损STM更能提高睾酮产量。与对照组相比,由于没有生殖细胞,STM中每个支持细胞的转铁蛋白分泌减少,但程度小于精母细胞和精子细胞的产生。总之,支持细胞分泌的参与调节睾丸间质细胞睾酮产生的旁分泌因子和转铁蛋白会因生殖细胞而发生改变。