Insights into differentiation and function of the transition region between the seminiferous tubule and rete testis

2021 ◽  
Author(s):  
A.F.A. Figueiredo ◽  
Rex A. Hess ◽  
S.R. Batlouni ◽  
N.T. Wnuk ◽  
A.O. Tavares ◽  
...  

Cell Cycle ◽  
2016 ◽  
Vol 15 (18) ◽  
pp. 2486-2496 ◽  
Author(s):  
A. F. A. Figueiredo ◽  
L. R. França ◽  
R. A. Hess ◽  
G. M. J. Costa


2019 ◽  
Vol 116 (9) ◽  
pp. 3584-3593 ◽  
Author(s):  
Shuiqiao Yuan ◽  
Yue Liu ◽  
Hongying Peng ◽  
Chong Tang ◽  
Grant W. Hennig ◽  
...  

Cilia are cell-surface, microtubule-based organelles that project into extracellular space. Motile cilia are conserved throughout eukaryotes, and their beat induces the flow of fluid, relative to cell surfaces. In mammals, the coordinated beat of motile cilia provides highly specialized functions associated with the movement of luminal contents, as seen with metachronal waves transporting mucus in the respiratory tract. Motile cilia are also present in the male and female reproductive tracts. In the female, wave-like motions of oviductal cilia transport oocytes and embryos toward the uterus. A similar function has been assumed for motile cilia in efferent ductules of the male—i.e., to transport immotile sperm from rete testis into the epididymis. However, we report here that efferent ductal cilia in the male do not display a uniform wave-like beat to transport sperm solely in one direction, but rather exert a centripetal force on luminal fluids through whip-like beating with continual changes in direction, generating turbulence, which maintains immotile spermatozoa in suspension within the lumen. Genetic ablation of two miRNA clusters (miR-34b/c and -449a/b/c) led to failure in multiciliogenesis in murine efferent ductules due to dysregulation of numerous genes, and this mouse model allowed us to demonstrate that loss of efferent duct motile cilia causes sperm aggregation and agglutination, luminal obstruction, and sperm granulomas, which, in turn, induce back-pressure atrophy of the testis and ultimately male infertility.



2002 ◽  
Vol 126 (1) ◽  
pp. 64-69
Author(s):  
Manuel Nistal ◽  
María Luisa Riestra ◽  
Ricardo Paniagua

Abstract Objective.—To evaluate seminiferous epithelium lesions in adult cryptorchid testes showing lymphoid infiltrates in seminiferous tubules and interstitium (ie, focal orchitis). Also, to consider the possible role of this lesion in the etiology of tubular atrophy. Methods.—We performed a histopathologic study of the cryptorchid testes and adjacent epididymides removed from 50 adult men who had not been previously treated for cryptorchidism. The study included morphologic and semiquantitative evaluation of seminiferous tubule pathology (according to germ cell numbers), Sertoli cell morphology, tubular lumen dilation, rete testis pattern (normal, hypoplastic, or cystic), and epididymal pattern (normal or epididymal duct hypoplasia). The study also included immunohistochemical evaluation of immune cell markers. The results were compared with clinical and laboratory findings. Results.—Focal lymphoid infiltrates (mainly lymphocytes) in seminiferous tubules and interstitium were found in 22 patients (44%), all of whom had unilateral cryptorchidism. The course of orchitis was asymptomatic, and laboratory data were normal. According to the seminiferous tubule pathology, a variety of histopathologic diagnoses, were made: (1) mixed atrophy consisting of Sertoli cell–only tubules intermingled with tubules showing maturation arrest of spermatogonia (11 testes, 4 of which also showed hyalinized tubules); (2) Sertoli cell–only tubules plus hyalinized tubules (4 testes); (3) Sertoli cell–only tubules (3 testes); (4) intratubular germ cell neoplasia (2 testes, 1 of which also showed hyalinized tubules); (5) complete tubular hyalinization (1 testis); and (6) tubular hyalinization plus some groups of tubules with hypospermatogenesis (all germ cell types were present although in lower numbers, 1 testis). Dysgenetic Sertoli cells, that is, Sertoli cells that had undergone anomalous, incomplete maturation, were observed in all nonhyalinized seminiferous tubules with inflammatory infiltrates. Tubular ectasia was observed in 13 cases. The rete testis was hypoplastic and showed cystic transformation in 18 testes, and the epididymis was hypoplastic in 15 testes. Conclusions.—The causes of these focal inflammatory infiltrates are unknown. It is possible that tubular ectasia and Sertoli cell dysgenesis are involved and that these alterations cause a disruption of the blood-testis barrier and allow antigens to enter the testicular interstitium, giving rise to an autoimmune process.



1985 ◽  
Vol 33 (5) ◽  
pp. 1245-1251 ◽  
Author(s):  
Karl E. Muffly ◽  
Terry T. Turner ◽  
Melinda Brown ◽  
Peter F. Hall


Reproduction ◽  
2011 ◽  
Vol 142 (1) ◽  
pp. 167-173 ◽  
Author(s):  
Charles L Bormann ◽  
Gary D Smith ◽  
Vasantha Padmanabhan ◽  
Theresa M Lee

Androgens play important roles during the first trimester of intrauterine life, coinciding with genital tract differentiation, during virilization and maintenance of secondary male characteristics, and during initiation of spermatogenesis. Little is known about the impact of inappropriate exposure to excess androgens during fetal development on male sexual maturation and reproduction. The objectives of this study were to determine the effects of prenatal 5α-dihydrotestosterone (DHT) and testosterone treatment during ovine sexual differentiation on post-pubertal testicular formation and subsequent potential for fertility as assessed by epididymal sperm characteristics. Rams prenatally treated with testosterone exhibited increased testicular weight relative to age-matched controls and prenatal DHT-treated rams (P<0.05), as well as elevated total and free testosterone concentrations compared with DHT-treated rams (P=0.07 and P<0.05 respectively). The percentage of progressively motile sperm from the epididymis was significantly reduced in prenatal DHT-treated but not testosterone-treated rams compared with control rams (P<0.05). The testosterone-treated rams had a greater number of germ cell layers than DHT-treated rams, but comparable to the controls. Prenatal testosterone-treated rams had significantly larger seminiferous tubule diameter and lumen diameter compared with prenatal DHT-treated (P<0.05). Significantly, more prenatal DHT- and testosterone-treated rams (P<0.05) had occluded tubule lumen than control rams. Findings from this study demonstrate that exposure to excess testosterone/DHT during male fetal sexual differentiation have differential effects on post-pubertal testicular size, seminiferous tubule size and function, sperm motility, and testosterone concentrations.



Author(s):  
Naohiro Sugita ◽  
Narantsog Choijookhuu ◽  
Koichi Yano ◽  
Deokcheol Lee ◽  
Makoto Ikenoue ◽  
...  

Abstract High-mobility group box 2 (HMGB2), a chromatin-associated protein that interacts with DNA, is implicated in multiple biological processes, including gene transcription, replication, and repair. HMGB2 is expressed in several tissues, including the testis; however, its functional role is largely unknown. Here, we elucidated the role of HMGB2 in spermatogenesis using HMGB2 knock-out (KO) mice. Paraffin-embedded testicular tissues were obtained from 8-week-old and 1-year-old wild-type and KO mice. Testis weight and number of seminiferous tubules were decreased, whereas atrophic tubules were increased in HMGB2-depleted mice. Immunohistochemistry revealed that atrophic tubules contained Sertoli cells, but not germ cells. Moreover, decreased cell proliferation and increased apoptosis were demonstrated in HMGB2-depleted mouse testis. To elucidate the cause of tubule atrophy, we examined the expression of androgen and estrogen receptors (AR, ERs, respectively), and the results indicated aberrant expression of AR and ERα in Sertoli and Leydig cells. Southwestern histochemistry detected decreased estrogen response element–binding sites in HMGB2-depleted mouse testis. Expression of HMGB1, which has highly similar structure and function as HMGB2, was examined by immunohistochemistry and western blotting, which indicated increased expression in aged HMGB2 KO mouse testis, especially in spermatocytes. These findings indicate a compensatory increase in HMGB1 expression in HMGB2 KO mouse testis. In summary, depletion of HMGB2 induced aberrant expression of AR and ERα, leading to decreased germ cell proliferation and increased apoptosis that resulted in focal seminiferous tubule atrophy.



Reproduction ◽  
2019 ◽  
Vol 158 (2) ◽  
pp. 201-211 ◽  
Author(s):  
André F A Figueiredo ◽  
Natália Teixeira Wnuk ◽  
Amanda O Tavares ◽  
José Rafael Miranda ◽  
Rex A Hess ◽  
...  

The number of Sertoli cells (SCs) ultimately determines the upper limit of sperm production in the testis. Previous studies have shown that thyroid hormones (TH) receptors are abundantly expressed in developing SCs; therefore, it was highly significant to discover that transient neonatal hypothyroidism induced by the goitrogen 6-n-propyl-2-thiouracil (PTU) can extend SCs proliferation beyond the first 2 weeks postnatal and increase testis weight and sperm production. Further studies concluded that treatment must begin before day 8 post birth in rats. Recent studies, however, showed that SCs present in the transition region at the rete testis exhibit a more immature phenotype and have prolonged mitotic activity, which led to the hypothesis that SCs in this region will retain the capacity to respond to PTU treatment over a longer period of time. In the present study, male Wistar rats were treated with PTU from days 21 to 40 and were evaluated at 40 and 160 days of age. Similar to neonatal rat SCs, it was demonstrated that prepubertal SCs in the transition region have a high mitotic activity and are highly sensitive to TH levels. This delayed, transient hypothyroidism resulted in significantly increased testis weight, SCs number and daily sperm production. The results demonstrate for the first time that Sertoli cells showing plasticity in the transition region can be stimulated to increase proliferation and contribute to a late stage surge in testis weight and sperm output.



Reproduction ◽  
1971 ◽  
Vol 27 (3) ◽  
pp. 463-465 ◽  
Author(s):  
A. I. KOSKIMIES ◽  
M. KORMANO ◽  
A. LAHTI


Reproduction ◽  
2002 ◽  
pp. 779-788 ◽  
Author(s):  
RA Anderson ◽  
N Cambray ◽  
PS Hartley ◽  
AS McNeilly

Inhibins and activins have roles in the regulation of cell proliferation and differentiation in a variety of tissues. This study investigated the distribution of the three inhibin/activin subunits (alpha, betaA and betaB) and their receptors in the human testis between week 13 and week 19 of gestation using RT-PCR and immunohistochemistry. mRNA for all three subunits and for the activin type II receptors ActRIIA and ActRIIB was detected at all stages of gestation examined. Sertoli cells showed intense immunostaining for the alpha subunit and some staining for the betaB subunit, whereas only the betaB subunit was detected in gonocytes. No betaA subunit staining was detected within the tubules. All three subunits were localized to interstitial Leydig cells. Cells of the rete testis and the epididymal epithelium also showed immunostaining for betaB; however, staining for the other subunits was weak or absent. Peritubular cells showed intense immunostaining for the beta-glycan inhibin receptor, which was also localized to interstitial cells, but was not detected within the tubular compartment, rete testis or epididymal epithelium. ActRIIA was detected in gonocytes and in interstitial cells; ActRIIB was distributed widely. These data indicate that fetal Leydig and Sertoli cells have the potential to produce both activins and inhibins, whereas gonocytes may produce only activin B. The distribution of activin and inhibin receptors implies that the intratubular compartment and developing duct system are sites of action of activin B but not inhibin at this stage of development, whereas both activins and inhibins may be involved in the development and function of the peritubular and interstitial cells.



Andrologia ◽  
2009 ◽  
Vol 14 (4) ◽  
pp. 352-362 ◽  
Author(s):  
S.G. LINDNER ◽  
A.F. HOLSTEIN


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