Disease relevance of Seminiferous Tubules

• However, premeiotic murine gametocytes lacked detectable Gas8 protein, as did seminiferous tubules in biopsy specimens from seven human males having cytological evidence of non-obstructive azoospermia secondary to Sertoli cell-only syndrome [1].
• Microscopic changes were restricted to the testes and the heart, and were seen only in males dosed with 1080 at 0.25 mg/kg/day and included severe hypospermia in the epididymides, severe degeneration of the seminiferous tubules of the testes, and cardiomyopathy [2].
• TP was given for 14 days (3 mg/100 g body weight, i.m.) to assess the acute effects of testosterone on the seminiferous tubules [3].
• Histopathological studies revealed marked degeneration of seminiferous tubules and lumen devoid of sperms, further confirming testicular toxicity of styrene [4].
• Other changes seen were the hyalinization of gastric submucosal wall, generalized testicular atrophy due to the loss of seminiferous tubules, coagulation necrosis of intestinal mucosal wall, hyperpigmentation, and more advanced and severe chronic progressive glomerulonephropathy in the TFE-treated rats [5].

High impact information on Seminiferous Tubules

• The GATA-1-expressing cells in 10-week-old testis were found only in contact with the basement membrane of seminiferous tubules, suggesting that GATA-1 regulates genes during the earliest stages of spermatogenesis [6].
• We use an anti-mGATA-1 monoclonal antibody to show that the factor expressed in erythroid cells is the same as that found in the seminiferous tubules of murine testis [6].
• Ovaries of adult alphabetaERKO females exhibit follicle transdifferentiation to structures resembling seminiferous tubules of the testis, including Sertoli-like cells and expression of Müllerian inhibiting substance, sulfated glycoprotein-2, and Sox9 [7].
• Immunoassay of androgen binding protein in blood: a new approach for study of the seminiferous tubule [8].
• While young Taf4b-null males are initially fertile, Taf4b-null males become infertile by 3 mo of age and eventually exhibit seminiferous tubules devoid of germ cells [9].

Chemical compound and disease context of Seminiferous Tubules

• These observations suggest that the segregation of testicular autoantigens in the luminal compartment of seminiferous tubules is not complete for all of them in the rat and emphasize the role of more dynamic mechanisms in prevention of anti-germ cell autoimmune disease [10].
• The 4-month exposure period to fluoride (200 microg/ml of drinking water) induced histopathological changes (hemorrhage in interstitium, necrosis and apoptosis in seminiferous tubule epithelium) which were accompanied by decreased testicular zinc concentration and increased lipid peroxidation [11].
• Histologically, torsion caused some separation between germinal cells in the seminiferous tubules, which became much more prominent in the detorsion group and attenuated with propofol pretreatment [12].
• Quail fed 20.0 or 10.0 ml formalin/kg feed showed depression, decreased responsiveness, feed consumption, and body weights, and had vacuolation in the germinal epithelial layer of their seminiferous tubules [13].
• In animals exposed to 5000 and 10,000 mg DEHP/kg b.wt. a severe atrophy of the seminiferous tubules and a slight diffuse Leydig's cell hyperplasia was observed [14].

Biological context of Seminiferous Tubules

• Findings are discussed in relation to the nature of mesenchymal-epithelial cell interactions in the seminiferous tubule and to the possible role of P Mod-S as a mediator of androgen actions of Sertoli cells [15].
• Histological analysis revealed that the round spermatids and the pachytene spermatocytes failed to attach to the Sertoli cells in the seminiferous tubules and sloughed off into the lumen with apoptosis in the Tslc1(-/-) mice [16].
• This phenotype could be linked to a defect(s) in germ cells and/or to inadequate Sertoli cell function, leading to seminiferous tubule disorganization and finally to a total disappearance of germ cells [17].
• CDK4(-/-) mice survived embryogenesis and showed growth retardation and reproductive dysfunction associated with hypoplastic seminiferous tubules in the testis and perturbed corpus luteum formation in the ovary [18].
• Further, the developmental stage-specific expression of I-CREBs in germ cells of the seminiferous tubules correlates with the cyclical down-regulation of activator CREB, suggesting that I-CREBs repress expression of the cAMP-inducible CREB gene as well as other genes transiently induced by cAMP during the 12-day cycle of spermatogenesis [19].

Anatomical context of Seminiferous Tubules

• Results are discussed with respect to the nature of interactions between mesenchymal peritubular cell precursors and adjacent epithelial Sertoli cell precursors in the formation of the basal lamina of the seminiferous tubule [20].
• Follitropin (FSH) is a pituitary glycoprotein hormone that is essential for the development of ovarian follicles and testicular seminiferous tubules [21].
• In older transgenic mice, abnormal accumulation of spermatogonia and degeneration of these germ cells was still observed, but some seminiferous tubules in which the level of Bcl-2 expression was reduced recovered normal spermatogenesis [22].
• Male Brca1(Delta11/Delta11)p53(+/-) mice that carried a homozygous deletion of Brca1 exon 11 and a p53 heterozygous mutation had significantly reduced testicular size and no spermatozoa in their seminiferous tubules [23].
• Disruption of blood-testis barrier on day 20 was evidenced by the detection of 1) perfused lanthanum deposits between Sertoli cells and surrounding inflammatory cells inside the seminiferous tubules, 2) deposits of endogenous mouse IgG in germinal epithelium, and 3) probable immune complexes (granular C3) surrounding seminiferous tubules [24].

Associations of Seminiferous Tubules with chemical compounds

• The testicular antiviral defense system: localization, expression, and regulation of 2'5' oligoadenylate synthetase, double-stranded RNA-activated protein kinase, and Mx proteins in the rat seminiferous tubule [25].
• A distinctive Mn-2+-sensitive adenylate cyclase [ATP pyrophosphate-lyase(cyclizing), EC 4.6.1.1] system insensitive to fluoride has been found in rat seminiferous tubules and epididymal sperm [26].
• Characterization of mutations induced by ethylnitrosourea in seminiferous tubule germ cells of transgenic B6C3F1 mice [27].
• To evaluate the role of apoptosis in human adult testes, apoptosis was induced in seminiferous tubules that were incubated under serum-free conditions in the absence or presence of testosterone [28].
• The effects on seminiferous tubule and Leydig cell function, as judged by serum FSH and LH concentrations, suggest that subtle Leydig cell dysfunction, in addition to germ cell depletion, may also occur at exposures greater than 200 rad [29].

Gene context of Seminiferous Tubules

• Cyclic expression of endothelin-converting enzyme-1 mediates the functional regulation of seminiferous tubule contraction [30].
• Dual control of seminiferous tubule contractility mediated by ETA and ETB endothelin receptor subtypes [31].
• In contrast, cycloheximide has little or no effect on the absorbance profiles and distribution of Rpl32 mRNA and 5' TOP mRNAs in adult seminiferous tubules [32].
• Additionally, we have localized HLA-E molecules on the cells of the adluminal compartment within seminiferous tubules using immunostaining with monoclonal antibodies specific for HLA-E heavy chain followed by confocal microscopy analysis [33].
• Small amounts of IGFBP-2 mRNA were expressed in seminiferous tubules, but none could be detected in liver [34].

Analytical, diagnostic and therapeutic context of Seminiferous Tubules

• Transgenic B6C3F1 mice carrying a lacI target gene were exposed to acute and multiple doses of ethylnitrosourea (ENU), and germ cells from the seminiferous tubules were assayed for mutation 3 and 90 days after treatment [27].
• Furthermore, THR alpha and its variant mRNA was found, using in situ hybridization, in the seminiferous cords and seminiferous tubules of fetal and prepubertal testis.(ABSTRACT TRUNCATED AT 250 WORDS)[35]
• Indirect immunofluorescence studies failed to demonstrate an immunoglobulin in the patients' sera that bound to Leydig cells or seminiferous tubules of normal adult human testes [36].
• The animals were decapitated on the third day after hypophysectomy, the testes were excised, and interstitial tissue was teased from seminiferous tubules before storage at -70 C until assayed [37].
• Northern blot hybridization to RNAs extracted from samples of seminiferous tubules at different stages of the epithelial cycle confirmed that expression of PACAP mRNA is restricted to specific stages of the cycle [38].

References