FSH Receptor (fsh + receptor)

Distribution by Scientific Domains


Selected Abstracts


Effects of FSH receptor deletion on epididymal tubules and sperm morphology, numbers, and motility

MOLECULAR REPRODUCTION & DEVELOPMENT, Issue 2 2005
Amit Grover
Abstract Follicle stimulating hormone (FSH) interacts with its cognate receptor (R) on Sertoli cells within the testis and plays an important role in the maintenance of spermatogenesis. Male FSH-R knockout (FORKO) mice show fewer Sertoli cells and many that are structurally abnormal and as a consequence fewer germ cells. Lower levels of serum testosterone (T) and androgen binding protein (ABP) also occur, along with reduced fertility. To assess the effects of FSH-R depletion as an outcome of testicular abnormalities, sperm from the cauda epididymidis were counted and examined ultrastructurally. As reduced fertility may also reflect changes to the epididymis, the secondary responses of the epididymis to lower T and ABP levels were also examined by comparing differences in sizes of epididymal tubules in various regions of FORKO and wild type (WT) mice. Sperm motility was evaluated in FORKO mice and compared to that of WT mice by computer assisted sperm analysis (CASA). Quantitatively, the data revealed that epithelial areas of the caput and corpus epididymidis were significantly smaller in FORKO mice compared to WT mice. Cauda epididymal sperm counts in FORKO mice were also much lower than in WT mice. This resulted in changes to 9 out of 14 sperm motility parameters, related mostly to velocity measures, which were significantly lower in the FORKO mice. The greatest change was observed relative to the percent static sperm, which was elevated by 20% in FORKO mice compared to controls. EM analyses revealed major changes to the structure of the heads and tails of cauda luminal sperm in FORKO mice. Taken together these data suggest a key role for the FSH receptor in maintaining Sertoli cells to sustain normal sperm numbers and proper shapes of their heads and tails. In addition, the shrinkage in epididymal epithelial areas observed in FORKO mice likely reflect direct and/or indirect changes in the functions of these cells and their role in promoting sperm motility, which is noticeably altered in FORKO mice. Mol. Reprod. Dev. © 2005 Wiley-Liss, Inc. [source]


Distribution and function of FSH receptor genetic variants in normal men

ANDROLOGIA, Issue 3 2002
K. Asatiani
Summary. Follicle stimulating hormone (FSH) plays a key role in the maintenance of qualitatively and quantitatively normal spermatogenesis. It controls gamete development through Sertoli cells, via binding to its receptor. The influence and importance of FSH receptor (FSHR) variants on Sertoli cell function is not completely understood and remains to be investigated. In this retrospective study, we explored the impact and action of two distinct FSHR isoforms, Thr307/Asn680 and Ala307/Ser680, in a large group of men. This investigation includes 288 normal healthy men, 86 of whom were proven fathers previously studied, and 202 were newly recruited subjects. The FSHR polymorphism at position 680 was analyzed in the whole group, while position 307 was investigated in 150 subjects, both of them by single-stranded conformation polymorphism (SSCP) gel electrophoresis. The distribution frequency for position 680 was 29% for the Asn/Asn, 52% for the Asn-Ser, 19% for the Ser-Ser variant, and for position 307, 27% for the Thr-Thr, 55% for the Ala-Thr, 18% for the Ala-Ala, respectively. Polymorphism combinations that were different from Thr307/Asn680 , Ala307/Ser680 were found in four subjects. When subjects were grouped according to genotype at position 680, no significant differences between basal FSH, testosterone, inhibin B levels and semen parameters were found. This clinical finding demonstrates that, differently from females, in whom a significant correlation between FSHR polymorphism and basal FSH levels was found, the FSHR genotype has no influence on clinical parameters in males. [source]


Autoantibodies against the FSH receptor: association or causation?

CLINICAL ENDOCRINOLOGY, Issue 4 2004
Lawrence C. Layman
No abstract is available for this article. [source]


Infancy is not a quiescent period of testicular development

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 1 2001
Héctor E. Chemes
Postnatal evolution of the testis in most laboratory animals is characterized by the close continuity between neonatal activation and pubertal development. In higher primates, infancy, a long period of variable duration, separates birth from the beginning of puberty. This period has been classically considered as a quiescent phase of testicular development, but is actually characterized by intense, yet inapparent activity. Testicular volume increases vigorously shortly after birth and in early infancy due to the growth in length of seminiferous cords. This longitudinal growth results from active proliferation of infantile Sertoli cells which otherwise display a unique array of functional capabilities (oestrogen and anti-müllerian hormone secretion, increase of FSH receptors and maximal response to FSH). Leydig cells also show recrudescence after birth, possibly determined by an active gonadotrophic-testicular axis which results in increased testosterone secretion of uncertain functional role. This postnatal activation slowly subsides during late infancy when periodic phases of activation of the hypothalamo-pituitary-testicular axis are paralleled by incomplete spermatogenic spurts. The beginning of puberty is marked by the simultaneous reawakening of Leydig cell function and succeeding phases of germ cell differentiation/degeneration which ultimately lead to final spermatogenic maturation. The marked testicular growth in this stage is due to progressive increase at seminiferous tubule diameter. Sertoli cells, which have reached mitotic arrest, develop and differentiate, establishing the seminiferous tubule barrier, fluid secretion and lumen formation, and acquiring cyclic morphological and metabolic variations characteristic of the mature stage. All of these modifications indicate that, far from being quiescent, the testis in primates experiences numerous changes during infancy, and that the potential for pubertal development and normal adult fertility depends on the successful completion of these changes. [source]


Gonadotrophin receptor blocking antibodies measured by the use of cell lines stably expressing human gonadotrophin receptors are not detectable in women with 46,XX premature ovarian failure

CLINICAL ENDOCRINOLOGY, Issue 3 2004
Massimo Tonacchera
Summary background, Premature ovarian failure (POF) is defined by cessation of ovarian function after puberty and before the age of 40. The syndrome is characterized by amenorrhoea, oestrogen deficiency and elevated levels of gonadotrophins. Autoimmunity has been proposed as a mechanism for some cases of destruction or malfunction of ovarian follicles. POF is often associated with type I and type II polyglandular autoimmune syndromes. It has also been postulated that receptors such as the LH and FSH receptors might become targets for blocking antibodies and such antibodies could be a cause of ovarian failure. patients and methods, Sixty-nine patients with POF isolated or associated with other endocrine autoimmune diseases (autoimmune thyroid diseases, Addison's disease, type 1 diabetes mellitus, multiple sclerosis, myasthenia gravis) were studied. All the patients had secondary amenorrhoea. The patient group had a median age of 33·1 years (range 15,57). Ovarian failure had been diagnosed at a median age of 29 years (range 15,39). The median time since diagnosis was almost 1 year but in six patients gonadal insufficiency had appeared 10,30 years earlier. All had a normal chromosomal karyotype (46, XX). Patients with POF were characterized by duration of amenorrhoea > 1 year, with elevated FSH and LH levels and undetectable or low oestrogen levels. Cell lines stably expressing recombinant human LH (CHO-LHr) and FSH (CHO-FSHr) receptors were prepared and used to search for antibodies able to inhibit LH- or FSH-stimulated cAMP production. Immunoglobulins extracted from sera of patients with POF were incubated with CHO-LHr and CHO-FSHr in the presence of human recombinant CG and FSH, respectively. results and conclusions, None of the immunoglobulin G (IgG) preparations from patients with POF was able to inhibit the activity of the FSH- and CG-stimulated cAMP production. [source]