Temperature and germ cell regulation of Leydig cell proliferation stimulated by Sertoli cell-secreted mitogenic factor: a possible role in cryptorchidism

Andrologia ◽  
2009 ◽  
Vol 28 (5) ◽  
pp. 247-257 ◽  
Author(s):  
N. Wu ◽  
E. P. Murono
Endocrine ◽  
1996 ◽  
Vol 5 (1) ◽  
pp. 75-83 ◽  
Author(s):  
Naixing Wu ◽  
Eisuke P. Murono ◽  
Wayne E. Carver ◽  
Louis Terracio ◽  
Thierry Bacro

2008 ◽  
Vol 132 (4) ◽  
pp. 548-564 ◽  
Author(s):  
Robert H. Young

Abstract The histopathology of testicular tumors is presented, emphasizing new, unusual, or underemphasized aspects. Within the category of seminoma of the usual type, the recent literature has drawn attention to the presence in occasional tumors of solid or hollow tubules or spaces of varying sizes and shape that may result in cribriform or microcystic patterns, causing potential confusion with other neoplasms, most notably Sertoli cell tumor or yolk sac tumor. Although regions of typical neoplasia and awareness of this phenomenon usually will be diagnostic, immunohistochemistry may play a role in excluding Sertoli cell tumor or yolk sac tumor. Although immunohistochemistry can play an undoubted helpful role in this and selected other areas of testicular tumor evaluation, careful evaluation of the gross and routine microscopic features will solve the vast majority of diagnostic problems. An excellent review of immunohistochemistry in this area by R. E. Emerson, MD, and T. M. Ulbright, MD, is cited herein. Spermatocytic seminoma remains a crucial pitfall in diagnosis, and the pathologist must always be alert to the possible diagnosis when looking at a seminomatous neoplasm, particularly in an older patient, although about one third of these tumors occur in the usual seminoma age range. The embryonal carcinoma has a great diversity of patterns, which are briefly noted. The enigmatic and picturesque tumor, polyembryoma, which virtually never occurs in pure form but may be a confusing component of a variety of mixed germ cell tumors, is discussed and illustrated. The phenomenon of burnt-out germ cell neoplasia is also briefly noted and an excellent recent contribution is referred to. Within the sex cord–stromal family of neoplasms, recent contributions and elaborations of unusual morphologic features of Leydig cell tumors and Sertoli cell tumors are presented. Within the Leydig cell family, cyst formation, adipose metaplasia, calcification or ossification, and spindle cell patterns may be particularly confusing, and in the Sertoli cell family, a great array of patterns caused by differing admixtures of tubular, solid, and stromal components occur. The peculiar lesion, intratubular large cell hyalinizing Sertoli cell tumor, of young boys with Peutz-Jeghers syndrome, is briefly discussed. Some of the problems in the family of hematopoietic neoplasms are reviewed, these processes posing diverse problems in differential diagnosis and their correct recognition having crucial therapeutic implications. Although secondary tumors to the testis have not received the same attention in the literature as the similar phenomenon in the female gonad, remarkable examples of testicular spread of diverse neoplasms, usually carcinoma but rarely melanoma, are seen, and the pathologist should be alert to this possibility, particularly when examining an unusual morphology in an older patient. Finally, a few comments are made on the common paratesticular neoplasm, the adenomatoid tumor, highlighting its varied patterns and recent description of some of the issues that may arise when they undergo total or subtotal infarction.


Endocrinology ◽  
1988 ◽  
Vol 122 (2) ◽  
pp. 749-755 ◽  
Author(s):  
ANDREA FABBRI ◽  
GAIL KNOX ◽  
ELLEN BUCZKO ◽  
MARIA L. DUFAU

2019 ◽  
Vol 33 (8) ◽  
pp. 9075-9086 ◽  
Author(s):  
Xiaohua Jiang ◽  
Shi Yin ◽  
Suixing Fan ◽  
Jianqiang Bao ◽  
Yuying Jiao ◽  
...  

2009 ◽  
Vol 42 (4) ◽  
pp. 291-303 ◽  
Author(s):  
M H Abel ◽  
D Baban ◽  
S Lee ◽  
H M Charlton ◽  
P J O'Shaughnessy

FSH acts through the Sertoli cell to ensure normal testicular development and function. To identify transcriptional mechanisms through which FSH acts in the testis, we have treated gonadotrophin-deficient hypogonadal (hpg) mice with recombinant FSH and measured changes in testicular transcript levels using microarrays and real-time PCR 12, 24 and 72 h after the start of treatment. Approximately 400 transcripts were significantly altered at each time point by FSH treatment. At 12 h, there was a clear increase in the levels of a number of known Sertoli cell transcripts (e.g. Fabp5, Lgals1, Tesc, Scara5, Aqp5). Additionally, levels of Leydig cell transcripts were also markedly increased (e.g. Ren1, Cyp17a1, Akr1b7, Star, Nr4a1). This was associated with a small but significant rise in testosterone at 24 and 72 h. At 24 h, androgen-dependent Sertoli cell transcripts were up-regulated (e.g. Rhox5, Drd4, Spinlw1, Tubb3 and Tsx) and this trend continued up to 72 h. By contrast with the somatic cells, only five germ cell transcripts (Dkkl1, Hdc, Pou5f1, Zfp541 and 1700021K02Rik) were altered by FSH within the time-course of the experiment. Analysis of canonical pathways showed that FSH induced a general decline in transcripts related to formation and regulation of tight junctions. Results show that FSH acts directly and indirectly to induce rapid changes in Sertoli cell and Leydig cell transcript levels in the hpg mouse but that effects on germ cell development must occur over a longer time-span.


2005 ◽  
Vol 186 (3) ◽  
pp. 429-446 ◽  
Author(s):  
Sarah J Meachem ◽  
Saleela M Ruwanpura ◽  
Jessica Ziolkowski ◽  
Jacquelyn M Ague ◽  
Michael K Skinner ◽  
...  

The critical influence of follicle stimulating hormone (FSH) on male fertility relates both to its impact on Sertoli cell proliferation in perinatal life and to its influence on the synthesis of Sertoli cell-derived products essential for germ cell survival and function in the developing adult testis. The nature and timing of this shift of germ cells to their reliance on specific Sertoli cell-derived products are not defined. Based on existing data, it is apparent that the dominant function of FSH shifts between 9 and 18 day postpartum (dpp) during the first wave of spermatogenesis from driving Sertoli cell proliferation to support germ cells. To enable comprehensive analysis of the impact of acute in vivo FSH suppression on Sertoli and germ cell development, FSH was selectively suppressed in Sprague–Dawley rats by passive immunisation for 2 days and/or 4 days prior to testis collection at 3, 9 and 18 dpp. The 3 dpp samples displayed no measurable changes, while 4 days of FSH suppression decreased Sertoli cell proliferation and numbers in 9 dpp, but not 18 dpp, animals. In contrast, germ cell numbers were unaffected at 9 dpp but decreased at 18 dpp following FSH suppression, with a corresponding increase in germ cell apoptosis measured at 18 dpp. Sixty transcripts were measured as changed at 18 dpp in response to 4 days of FSH suppression, as assessed using Affymetrix microarrays. Some of these are known as Sertoli cell-derived FSH-responsive genes (e.g. StAR, cathepsin L, insulin-like growth factor binding protein-3), while others encode proteins involved in cell cycle and survival regulation (e.g. cyclin D1, scavenger receptor class B 1). These data demonstrate that FSH differentially affects Sertoli and germ cells in an age-dependent manner in vivo, promoting Sertoli cell mitosis at day 9, and supporting germ cell viability at day 18. This model has enabled identification of candidate genes that contribute to the FSH-mediated pathway by which Sertoli cells support germ cells.


1996 ◽  
Vol 151 (1) ◽  
pp. 37-48 ◽  
Author(s):  
J Singh ◽  
D J Handelsman

Abstract We previously demonstrated that androgens alone, in the complete absence of gonadotropins, initiated qualitatively complete spermatogenesis in hypogonadal (hpg) mice. Although germ cell to Sertoli cell ratios were normal in hpg mice with androgen-induced spermatogenesis, testicular size, Sertoli cell and germ cell numbers only reached 40% of those of non-hpg mice, and Sertoli cell numbers were unaffected by androgen treatment started at 21 days of age. We postulated that these observations were due to diminished gonadotropin-dependent Sertoli cell proliferation during perinatal life while the Sertoli cells still exhibited normal carrying capacity for mature germ cells. In order to test this hypothesis, we examined the effects of administering androgens and gonadotropins to hpg mice during the first 2 weeks of postnatal life when Sertoli cells normally continue to proliferate. The study end-points were Sertoli and germ cell numbers in hpg mice following induction of spermatogenesis by 8 weeks treatment with 1 cm subdermal silastic testosterone implants. Newborn pups (postnatal day 0–1) were injected s.c. with recombinant human FSH (rhFSH) (0·5 IU/20 μl) or saline once daily for 14 days, with or without a single dose of testosterone propionate (TP) (100 μg/20 μl arachis oil) or human chorionic gonadotropin (hCG) (1 IU/20 μl). Untreated hpg and phenotypically normal littermates were studied as concurrent controls. At 21 days of age, all treated weanling mice received a 1 cm silastic subdermal testosterone implant and, finally, 8 weeks after testosterone implantation, all mice were killed. As expected, qualitatively complete spermatogenesis was induced in all groups by testosterone despite undetectable circulating FSH levels. Exogenous rhFSH increased testis size by 43% (P<0·002) but a single neonatal dose of either TP or hCG reduced the FSH effect although neither TP nor hCG had any effect alone. In contrast, a single neonatal dose of TP or hCG increased final seminal vesicle size whereas FSH had no effect. FSH and TP treatment significantly increased absolute numbers of testicular spermatids compared with saline treatment, whereas hCG and TP significantly increased testicular sperm when expressed relative to testis size. Stereological evaluation of Sertoli and germ cell numbers demonstrated a rise in the absolute numbers of Sertoli and all germ cell populations induced by neonatal administration of hormones. When expressed per Sertoli cells the numbers of germ cells in the treated mice were between 85 and 90% of non-hpg controls. We conclude that exogenous FSH treatment during the first 2 weeks of postnatal life, coinciding with the natural time of Sertoli cell proliferation, increases Sertoli cell numbers and thereby the ultimate size of the mature testis and its germ cell production. Thus neonatal gonadotropin secretion may be a critical determinant of the sperm-producing capacity of the mature testis. In addition, neonatal exposure to androgens could be important for the imprinting of sex accessory organs in hpg mice, with the long-term effects of altering the sensitivity of the accessory organs to exogenous testosterone later in life. Journal of Endocrinology (1996) 151, 37–48


1990 ◽  
Vol 4 (3) ◽  
pp. 393-401 ◽  
Author(s):  
Barbara J. Stallard ◽  
Michael D. Griswold

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