Dysplastic development of seminiferous tubules and interstitial tissue in rat hypogonadic (hgn/hgn) testes.
The hypogonadic rat is characterized by male sterility, reduced female fertility, and renal hypoplasia controlled by a single recessive allele (hgn) on chromosome 10. Plasma testosterone is low and levels of gonadotropins are high in adult male hgn/hgn rats, indicating that the cause of hypogonadism lies within the testis itself. We found that the postnatal growth of the seminiferous tubules was severely affected. Here we describe the details of postnatal testicular pathogenesis of the hgn/ hgn rats. In these rats, gonadal sex determination and initial differentiation of each type of testicular cell occur, but proliferation, differentiation, and maturation of these cells during postnatal testicular development is severely affected. Postnatal pathological changes include reduced proliferation and apoptotic cell death of Sertoli cells, abnormal mitosis and cell death of gonocytes, reduced deposition of extracellular matrix proteins into the basal lamina, lack of the formation of an outer basal lamina, formation of multiple layers of undifferentiated peritubular cells, and the delayed appearance and islet conformation of adult-type Leydig cells. Apoptotic cell death of Sertoli cells and disappearance of FSH receptor mRNA expression indicate that this mutant rat is a useful model for Sertoli cell dysfunction. The abnormalities listed above might be caused by defective interactions between Sertoli cells and other types of testicular cells. Because the results presented here strongly indicate that a normal allele for hgn encodes a factor playing a critical role in testicular development, the determination of the gene responsible for hgn and the analysis of early alterations of gene expression caused by mutations in this gene would provide important information on the mechanisms of testicular development.
Suzuki
Hiroetsu
H
Department of Veterinary Physiology, Nippon Veterinary and Animal Science University, Musashino-shi, Tokyo 180-8602, Japan. hiroetsu@nvau.ac.jp
Yagi
Mio
M
Saito
Kenichi
K
Suzuki
Katsushi
K
D015096:3-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000015:Abnormalities, Multiple / Q000209:etiology*; D000818:Animals; D017209:Apoptosis; D002452:Cell Count; D002455:Cell Division; D003598:Cytoskeletal Proteins / Q000378:metabolism; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D006651:Histocytochemistry; D007006:Hypogonadism / Q000150:complications* / Q000235:genetics* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D051381:Rats; D011922:Rats, Mutant Strains; D011962:Receptors, FSH / Q000378:metabolism; D012671:Seminiferous Tubules / Q000002:abnormalities* / Q000378:metabolism / Q000473:pathology; D013194:Staining and Labeling; D013737:Testis / Q000002:abnormalities* / Q000378:metabolism / Q000473:pathology; D014018:Tissue Distribution
D003598:Cytoskeletal Proteins; D016326:Extracellular Matrix Proteins; D011962:Receptors, FSH; D015096:3-Hydroxysteroid Dehydrogenases