Androgen receptor distribution in rat testis: new implications for androgen regulation of spermatogenesis.
Androgen receptor distribution in rat testis: new implications for androgen regulation of spermatogenesis.
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DOI：
10.1210/endo.134.5.8156934
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发表时间：
1994-05
期刊：
影响因子：
4.8
通讯作者：
W. Vornberger;G. Prins;N. Musto;C. Suárez‐Quian
中科院分区：
文献类型：
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作者：
W. Vornberger;G. Prins;N. Musto;C. Suárez‐Quian
用生物素-链亲和素免疫过氧化物酶测定雄激素受体（AR）在成年大鼠睾丸中的分布，采用包埋在聚酯蜡中的组织，在不影响组织保存的情况下保留抗原性。所使用的抗体探针是一种亲和纯化的兔多克隆抗体，对大鼠AR的氨基端肽进行表达。在间质室内，在一些间质细胞和所有形成血管壁的平滑肌细胞中检测到AR免疫染色，但血管内皮细胞呈阴性。此外，在那些被明确鉴定为AR免疫染色的间质细胞中，反应的强度各不相同。在精小管中，所有小管周围的肌样细胞核均可见AR免疫染色，但淋巴内皮细胞远端层未见。在支持细胞中，核AR免疫染色具有分期特异性。中度AR免疫染色首先在周期的IV期晚期或V期早期变得明显，在viii - viii期达到强劲的峰值，然后完全消失。特异性AR免疫染色也可在XI期伸长精子细胞的细胞核中发现，这些精子细胞的细胞核明显伸长，但染色质尚未开始凝聚。其次，随着染色质凝聚的发生，细胞核AR免疫染色在细长精子中没有发现，同时在生殖细胞的细胞质中也没有发现。这些结果可以用以下方式解释：1)间质细胞中AR的存在与雄激素以自分泌方式改变间质细胞活性的假设一致。此外，并非所有间质细胞在稳定状态下都表现出AR免疫染色，这表明这些细胞在群体中具有不同的功能活性。2)间质平滑肌细胞的强AR免疫染色表明这些细胞是雄激素的靶点。3)支持细胞和小管周围肌样细胞的AR免疫反应性表明它们参与了雄激素对精子发生的控制。然而，支持细胞的分期特异性AR免疫反应性可能更多地指示了这些阶段的特异性雄激素反应，而小管周围细胞可能参与精子发生的音调维持。4) AR在第11步细长精子中的特异性存在可能提示雄激素可以直接作用于生殖细胞调节精子发生。
The distribution of the androgen receptor (AR) in the adult rat testis was determined by biotin-streptavidin immunoperoxidase, employing tissue embedded in polyester wax which preserves antigenicity without compromising tissue preservation. The antibody probe used, which has been characterized previously, was an affinity purified, rabbit polyclonal antibody raised to the amino terminus peptide of the rat AR. Within the interstitial compartment, AR immunostaining was detected in some Leydig cells and all smooth muscle cells forming the walls of blood vessels, but endothelial cells of blood vessels were negative. Furthermore, in those Leydig cells that were clearly identified as exhibiting AR immunostaining, the intensity of the reaction varied. In the seminiferous tubules AR immunostaining was observed in all peritubular myoid cell nuclei, but not in the distal layer of lymphatic endothelial cells. In Sertoli cells, nuclear AR immunostaining was stage specific. Moderate AR immunostaining first became evident at late stage IV or early stage V of the cycle, reached a robust peak at stages VII-VIII, and then disappeared completely. Specific AR immunostaining was also discerned in the nuclei of stage XI elongated spermatids, the spermatids in which nuclear elongation is apparent but chromatin condensation has not yet begun. Next, with onset of chromatin condensation, nuclear AR immunostaining in elongated spermatids was not discerned concomitant with its detection in the cytoplasm of the germ cells. These results are interpreted in the following manner: 1) The presence of AR in Leydig cells is consistent with the hypothesis that androgens modify Leydig cell activity in an autocrine fashion. Further, that not all Leydig cells exhibited AR immunostaining at steady state suggests a differential, functional activity of these cells within the population. 2) The intense AR immunostaining of smooth muscle cells present in the interstitium indicates that these cells are targets for androgens. 3) AR immunoreactivity in both Sertoli and peritubular myoid cells suggests their involvement in the androgenic control of spermatogenesis. The stage specific AR immunoreactivity in Sertoli cells, however, may be more indicative of a specific androgen response during these stages, whereas peritubular cells may participate in the tonal maintenance of spermatogenesis. 4) The specific presence of AR in step 11 elongated spermatids may suggest that androgens can act directly on germ cells to regulate spermatogenesis.