JUNCTION-RELATED SERTOLI-CELL CYTOSKELETON IN TESTOSTERONE-TREATED HYPOPHYSECTOMIZED RATS

JUNCTION-RELATED SERTOLI-CELL CYTOSKELETON IN TESTOSTERONE-TREATED HYPOPHYSECTOMIZED RATS
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DOI:
10.1095/biolreprod49.5.1122
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发表时间:
1993-11-01
影响因子:
3.6
通讯作者:
CAMERON, DF
CAMERON, DF
中科院分区:
生物学2区
文献类型:
--
作者:
MUFFLY, KE;NAZIAN, SJ;CAMERON, DF

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睾酮是保证正常精子发生所必需的主要激素。然而,它在精子细胞成熟过程中的确切作用尚不清楚。在垂体切除的大鼠中,如果在手术后不久补充睾酮,就可以维持精子的生成。延迟治疗会导致成熟精子细胞数量的减少,在培养中,睾丸激素和FSH需要最大限度地使精子细胞与具有结合能力的Sertoli细胞附着。这种结合事件是精子发生过程中的一个重要步骤,并依赖于支持细胞细胞骨架的成分。本研究测定了去垂体大鼠睾丸激素即时替代和延迟替代后支持细胞的结合能力及其与精子细胞的连接相互作用。接受立即睾酮替代治疗的下丘脑切除大鼠周围分布有Sertoli细胞f-肌动蛋白和vinculin,结构完整的Sertoli胞浆特化面对Step 8精子细胞,每日精子产量与完整对照组观察到的这些参数相似。在延迟治疗组,这些参数是异常的,与未治疗的垂体切除动物的观察结果相似。这些结果表明,睾酮可以维持支持细胞的结合能力和正常的支持-精子细胞连接作用,但不能恢复它们。
Testosterone is the principal hormone necessary for insuring the completion of normal spermatogenesis. However, its precise role in spermatid maturation is not clear. In hypophysectomized rats, testosterone can maintain spermiogenesis if replaced soon after surgery. Delaying treatment results in a reduction in the number of mature spermatids, in culture, testosterone and FSH are required to maximize spermatid attachment to binding-competent Sertoli cells. This binding event is an essential step in the process of spermiogenesis and is dependent on components of the Sertoli cell cytoskeleton. The present study was undertaken to determine the binding competency of Sertoli cells and their junctional interaction with spermatids in the hypophysectomized rat after immediate testosterone replacement and after delayed testosterone replacement. Hypophysectomized rats treated with immediate testosterone replacement had peripheral distribution of Sertoli cell f-actin and vinculin, structurally intact Sertoli ectoplasmic specializations facing step 8 spermatids, and daily sperm production similar to these parameters as observed in intact controls. In the delayed treatment group, these parameters were abnormal and were similar to those observed in the untreated hypophysectomized animals. The results suggest that testosterone can maintain binding competency of the Sertoli cell and normal Sertoli-spermatid junctional interaction but cannot restore them.