scholarly journals Spermatogenesis and Sertoli Cell Activity in Mice Lacking Sertoli Cell Receptors for Follicle-Stimulating Hormone and Androgen

Endocrinology ◽  
2008 ◽  
Vol 149 (7) ◽  
pp. 3279-3285 ◽  
Author(s):  
M. H. Abel ◽  
P. J. Baker ◽  
H. M. Charlton ◽  
A. Monteiro ◽  
G. Verhoeven ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Hormonal Regulation ◽  
Cell Function ◽  
Cell Activity ◽  
Cell Number ◽  
Androgen Ablation ◽  
Specific Transcript ◽  
Synergistic Regulation ◽  
Hormonal Action ◽  
Failure To Progress

Spermatogenesis in the adult male depends on the action of FSH and androgen. Ablation of either hormone has deleterious effects on Sertoli cell function and the progression of germ cells through spermatogenesis. In this study we generated mice lacking both FSH receptors (FSHRKO) and androgen receptors on the Sertoli cell (SCARKO) to examine how FSH and androgen combine to regulate Sertoli cell function and spermatogenesis. Sertoli cell number in FSHRKO-SCARKO mice was reduced by about 50% but was not significantly different from FSHRKO mice. In contrast, total germ cell number in FSHRKO-SCARKO mice was reduced to 2% of control mice (and 20% of SCARKO mice) due to a failure to progress beyond early meiosis. Measurement of Sertoli cell-specific transcript levels showed that about a third were independent of hormonal action on the Sertoli cell, whereas others were predominantly androgen dependent or showed redundant control by FSH and androgen. Results show that FSH and androgen act through redundant, additive, and synergistic regulation of spermatogenesis and Sertoli cell activity. In addition, the Sertoli cell retains a significant capacity for activity, which is independent of direct hormonal regulation.

Cultured Sertoli cell-mediated FSH stimulatory effect on Leydig cell steroidogenesis

1985 ◽  
Vol 248 (2) ◽  
pp. E176-E181
Author(s):  
M. Benahmed ◽  
J. Reventos ◽  
E. Tabone ◽  
J. M. Saez
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Cell Function ◽  
Cell Activity ◽  
Defined Medium ◽  
Cell Number ◽  
Two Parameters ◽  
Leydig Cell Function

To determine the precise role of Sertoli cells in the stimulating effects of follicle stimulating hormone (FSH) on Leydig cell activity, porcine purified Leydig and Sertoli cells were cultured separately or together in a chemically defined medium in the absence or presence of porcine, FSH 50 ng/ml. Leydig cell activity was evaluated using two parameters: human chorionic gonadotropin (hCG) binding sites; and hCG-stimulated cAMP production and testosterone secretion. First, it was found that FSH increases Leydig cell activity in crude Leydig cell preparations (40–60% of Leydig cells), whereas it exerts no effect on purified Leydig cells (greater than 90% of Leydig cells). Second, FSH stimulates the activity of Leydig cells cocultured with Sertoli cells, whereas it remains without effect on purified Leydig cells cultured alone. This stimulating effect of FSH on Leydig cell activity is dependent on the Sertoli cell number in the coculture. These data 1) show that the stimulating effect of FSH on Leydig cell function is mediated by Sertoli cells and 2) support the concept of local control of Leydig cell function originating from Sertoli cells.

scholarly journals New perspectives in the diagnosis of pediatric male hypogonadism: the importance of AMH as a Sertoli cell marker

2011 ◽  
Vol 55 (8) ◽  
pp. 512-519 ◽  
Author(s):  
Romina P. Grinspon ◽  
Rodolfo A. Rey
Keyword(s):  
Sertoli Cell ◽  
Cell Function ◽  
Cell Activity ◽  
Tanner Stage ◽  
Inhibitory Effect ◽  
Male Hypogonadism ◽  
Fetal Life ◽  
Infancy And Childhood ◽  
Stimulation Tests ◽  
Enzyme Defects

Sertoli cells are the most active cell population in the testis during infancy and childhood. In these periods of life, hypogonadism can only be evidenced without stimulation tests, if Sertoli cell function is assessed. AMH is a useful marker of prepubertal Sertoli cell activity and number. Serum AMH is high from fetal life until mid-puberty. Testicular AMH production increases in response to FSH and is potently inhibited by androgens. Serum AMH is undetectable in anorchidic patients. In primary or central hypogonadism affecting the whole gonad and established in fetal life or childhood, serum AMH is low. Conversely, when hypogonadism affects only Leydig cells (e.g. LHβ mutations, LH/CG receptor or steroidogenic enzyme defects), serum AMH is normal or high. In pubertal males with central hypogonadism, AMH is low for Tanner stage (reflecting lack of FSH stimulus), but high for the age (indicating lack of testosterone inhibitory effect). Treatment with FSH provokes an increase in serum AMH, whereas hCG administration increases testosterone levels, which downregulate AMH. In conclusion, assessment of serum AMH is helpful to evaluate gonadal function, without the need for stimulation tests, and guides etiological diagnosis of pediatric male hypogonadism. Furthermore, serum AMH is an excellent marker of FSH and androgen action on the testis.

scholarly journals Cellular and molecular responses of adult testis to changes in nutrition: novel insights from the sheep model

Reproduction ◽  
2017 ◽  
Vol 154 (5) ◽  
pp. R133-R141 ◽  
Author(s):  
Yongjuan Guan ◽  
Graeme B Martin
Keyword(s):  
Germ Cell ◽  
Sertoli Cell ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Cell Number ◽  
Sheep Model ◽  
Germ Cell Apoptosis ◽  
Testis Regression ◽  
Male Sheep

This review explores the cellular and molecular mechanisms that regulate spermatogenesis in the post-pubertal testis that is regressing in response to mild undernutrition, using the sexually mature male sheep as a model. Testis regression leads to reductions in daily sperm production and in the quality of ejaculated spermatozoa (poorer movement, DNA damage). There is also a reduction in spermatogenic efficiency that appears to be caused, at least partially, by increases in germ cell apoptosis. Sertoli cell number does not change with testis regression, although about 1% of Sertoli cells do appear to retain proliferative ability after puberty. On the other hand, Sertoli cell function is disrupted during testis regression, as evidenced by a disorganization of tight junctions and indications that cell differentiation and maturation are reversed. Disrupted Sertoli cell function can explain, at least partially, the increase in germ cell apoptosis and any decrease in the rate of spermatogenesis, the two major contributors to spermatogenic efficiency. These outcomes seem to be mediated by changes in two RNA-based processes: (i) the expression of small non-coding RNAs that are involved in the regulation of Sertoli cell function, spermatogenesis and germ cell apoptosis and (ii) alternative pre-mRNA splicing that affects the regulation of spermatogenesis but does not appear to affect germ cell apoptosis, at least during testis progression induced by undernutrition in the male sheep. These research outcomes can be extended to other animal models and are relevant to issues in human male fertility.

High glucose levels affect spermatogenesis: an in vitro approach

2017 ◽  
Vol 29 (7) ◽  
pp. 1369 ◽  
Author(s):  
Renata S. Tavares ◽  
Joana M. D. Portela ◽  
Maria I. Sousa ◽  
Paula C. Mota ◽  
João Ramalho-Santos ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
High Glucose ◽  
Male Fertility ◽  
Cell Function ◽  
Post Partum ◽  
Cell Number ◽  
Glucose Levels ◽  
Clinical Complications

Besides known factors that may cause male infertility, systemic diseases such as diabetes mellitus may further exacerbate a decline in male fertility. This metabolic disease, clinically characterised by a hyperglycaemic phenotype, has devastating consequences in terms of human health, with reproductive dysfunction being one of the associated clinical complications. Nonetheless, the mechanisms responsible for such alterations are still poorly understood due to the multiplicity of factors involved in the induced pathophysiological changes. With this in mind, we focused on the main mediator of diabetes-associated alterations and performed an in vitro approach to address the effects of high glucose conditions on spermatogenesis, avoiding other confounding in vivo factors. Mouse (5 days post partum) testis fragments were cultured on agar gel stands at a gas–liquid interface with either 5, 25 or 50 mM D-glucose for 3 weeks. Stereological analysis revealed that high D-glucose levels increased Sertoli cell number (P < 0.05) and decreased tubular luminal area (P < 0.01), suggesting an impairment of this somatic cell type. Moreover, higher proliferative activity in a TM4 Sertoli cell line exposed to high D-glucose was found (P < 0.05) without compromising cell viability (P > 0.05), further suggesting altered Sertoli cell maturation. Overall, high D-glucose concentrations may lead to impairment of Sertoli cell function, which, given their significant role in spermatogenic control, may compromise male fertility.

scholarly journals Octreotide inhibits the enterochromaffin-like cell but not peroxisome proliferator-induced hypergastrinemia

2000 ◽  
Vol 25 (1) ◽  
pp. 109-119 ◽  
Author(s):  
I Bakke ◽  
AK Sandvik ◽  
HL Waldum
Keyword(s):  
Cell Function ◽  
Histidine Decarboxylase ◽  
Cell Activity ◽  
Cell Number ◽  
Peroxisome Proliferator ◽  
Cell Hyperplasia ◽  
Gastrin Cells ◽  
Gastrin Cell ◽  
Octreotide Lar ◽  
Ecl Cell

The peroxisome proliferator ciprofibrate induces hypergastrinemia and as a consequence, enterochromaffin-like (ECL) cell hyperplasia. The mechanism for the gastrin cell stimulation is unknown. The somatostatin analog octreotide LAR (long-acting release) was used to see if the stimulating effects of ciprofibrate could be attenuated. Female Fischer rats were dosed with ciprofibrate (50 mg/kg body weight per day) alone or combined with octreotide LAR (10 mg/30 days) for 60 days. Plasma gastrin and histamine, gastric endocrine cell densities and mRNA abundances were measured. Ciprofibrate increased gastrin mRNA abundance (P<0.05), gastrin cell number (P<0. 001) and cell area (P<0.01), and induced hypergastrinemia (P<0.001). These rats had profound ECL cell hyperplasia, confirmed by an increase in chromogranin A (CgA) and histidine decarboxylase (HDC) mRNA, density of neuroendocrine and ECL cells and plasma histamine levels (all P<0.001). Octreotide LAR did not affect ciprofibrate stimulation of gastrin cells, but all parameters of ECL cell hyperplasia were reduced (P<0.001). Octreotide LAR also significantly inhibited basal ECL cell function and growth. Ciprofibrate stimulates gastrin cell activity by a mechanism unaffected by octreotide, but octreotide does inhibit basal and gastrin-stimulated ECL cell function and growth.

scholarly journals Hormonal regulation of Sertoli cell function in the rat

1978 ◽  
Vol 18 (2B) ◽  
pp. 565-572 ◽  
Author(s):  
V. HANSSON ◽  
K. PURVIS ◽  
E. M. RITZÉN ◽  
F. S. FRENCH
Keyword(s):  
Sertoli Cell ◽  
Hormonal Regulation ◽  
Cell Function

Effect of an Extracellular Matrix on the Hormonal Regulation of Sertoli Cell Function

1987 ◽  
Vol 513 (1 Cell Biology) ◽  
pp. 413-414
Author(s):  
CATHERINE T. ANTHONY ◽  
BYRON K. GLENN ◽  
MICHAEL K. SKINNER
Keyword(s):  
Extracellular Matrix ◽  
Sertoli Cell ◽  
Hormonal Regulation ◽  
Cell Function

scholarly journals Effect of germ cell depletion on levels of specific mRNA transcripts in mouse Sertoli cells and Leydig cells

Reproduction ◽  
2008 ◽  
Vol 135 (6) ◽  
pp. 839-850 ◽  
Author(s):  
P J O'Shaughnessy ◽  
L Hu ◽  
P J Baker
Keyword(s):  
Germ Cell ◽  
Somatic Cell ◽  
Sertoli Cell ◽  
Germ Cells ◽  
Leydig Cell ◽  
Cell Function ◽  
Cell Activity ◽  
Cell Depletion ◽  
Transcript Levels ◽  
Mrna Transcripts

It has been shown that testicular germ cell development is critically dependent upon somatic cell activity but, conversely, the extent to which germ cells normally regulate somatic cell function is less clear. This study was designed, therefore, to examine the effect of germ cell depletion on Sertoli cell and Leydig cell transcript levels. Mice were treated with busulphan to deplete the germ cell population and levels of mRNA transcripts encoding 26 Sertoli cell-specific proteins and 6 Leydig cell proteins were measured by real-time PCR up to 50 days after treatment. Spermatogonia were lost from the testis between 5 and 10 days after treatment, while spermatocytes were depleted after 10 days and spermatids after 20 days. By 30 days after treatment, most tubules were devoid of germ cells. Circulating FSH and intratesticular testosterone were not significantly affected by treatment. Of the 26 Sertoli cell markers tested, 13 showed no change in transcript levels after busulphan treatment, 2 showed decreased levels, 9 showed increased levels and 2 showed a biphasic response. In 60% of cases, changes in transcript levels occurred after the loss of the spermatids. Levels of mRNA transcripts encoding Leydig cell-specific products related to steroidogenesis were unaffected by treatment. Results indicate (1) that germ cells play a major and widespread role in the regulation of Sertoli cell activity, (2) most changes in transcript levels are associated with the loss of spermatids and (3) Leydig cell steroidogenesis is largely unaffected by germ cell ablation.

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