Androgen receptor distribution in rat testis: new implications for androgen regulation of spermatogenesis.
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.
Vornberger
W
W
Department of Cell Biology, Georgetown University Medical Center, Washington, D.C. 20007.
Prins
G
G
Musto
N A
NA
Suarez-Quian
C A
CA
D000728:Androgens / Q000502:physiology*; D000818:Animals; D001426:Bacterial Proteins; D001710:Biotin; D002843:Chromatin / Q000648:ultrastructure; D003593:Cytoplasm / Q000648:ultrastructure; D004730:Endothelium, Vascular / Q000737:chemistry; D015151:Immunoblotting; D007124:Immunoenzyme Techniques; D007985:Leydig Cells / Q000737:chemistry; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000737:chemistry; D051381:Rats; D011944:Receptors, Androgen / Q000032:analysis*; D012671:Seminiferous Tubules / Q000737:chemistry; D012708:Sertoli Cells / Q000737:chemistry; D013087:Spermatids / Q000737:chemistry / Q000648:ultrastructure; D013091:Spermatogenesis; D019809:Streptavidin; D013737:Testis / Q000737:chemistry* / Q000502:physiology; D014018:Tissue Distribution
D000728:Androgens; D001426:Bacterial Proteins; D002843:Chromatin; D011944:Receptors, Androgen; D001710:Biotin; D019809:Streptavidin