311. Adult Sertoli cells proliferate in response to exogenous follicle stimulating hormone in the adult photo-inhibited Djungarian hamster

2005 ◽  
Vol 17 (9) ◽  
pp. 133
Author(s):  
G. A. Tarulli ◽  
P. G. Stanton ◽  
S. J. Meachem
Keyword(s):  
Cell Proliferation ◽  
Tight Junction ◽  
Sertoli Cell ◽  
Cell Population ◽  
Sertoli Cells ◽  
Follicle Stimulating Hormone ◽  
Tight Junction Proteins ◽  
Djungarian Hamster ◽  
Junction Proteins ◽  
Blood Testis Barrier

Sperm production relies on nutritional and structural support from Sertoli cells. Sertoli cells undergo maturational changes (e.g. cessation of proliferation and formation of the blood–testis barrier) around the onset of puberty in higher mammals1 and maturational failure has been associated with some infertility syndromes and testicular malignancies2. The Sertoli cell population is considered to be stable and unmodifiable by hormones after puberty in mammals, although recent data using the adult Djungarian hamster showed that Sertoli cell numbers decreased by 35% in the absence of serum gonadotrophins, and returned to control levels by short-term replacement of follicle stimulating hormone (FSH)3. Therefore, the aims of this study were to (i) quantify the proliferative activity of Sertoli cells in the hormonally manipulated Djungarian hamster, and (ii) examine the localisation of several tight junction proteins as markers of the blood–testis barrier. Long day (LD) photoperiod (16L : 8D) adult hamsters were exposed to short day (SD) photoperiod (8L : 16D) for 11 weeks to suppress gonadotrophins and then received FSH for up to 10 days. Sertoli cell proliferation was assessed immunohistochemically by the colocalisation of GATA-4 and PCNA, and quantified by stereology. Tight junction proteins (occludin and ZO-1) were colocalised using confocal microscopy. Sertoli cell proliferation in both the LD and SD controls was minimal; however, in response to FSH treatment proliferation was upregulated within 4 days compared with SD controls (98% v. 2%, P < 0.001, respectively). Tight junction proteins colocalised at the blood–testis barrier in LD hamsters, but were disorganised within the Sertoli cell cytoplasm in SD animals. FSH treatment restores colocalisation in a time-dependent manner. It is concluded that FSH contributes to the regulation of Sertoli cell proliferation and tight junction formation in the adult Djungarian hamster. This data provides definitive evidence that the adult Sertoli cell population in this model is modifiable by hormones. (1)Meachem et al. (2005). Biol Reprod 72, 1187.(2)Allan et al. (2004). Endocrinol 145, 1587.(3)Russell and Peterson (1985). Int Rev Cytol 94, 177.

002.Sertoli cell terminal differentiation: doing a 'U' turn on a one way street

2005 ◽  
Vol 17 (9) ◽  
pp. 62
Author(s):  
S. J. Meachem
Keyword(s):  
Cell Proliferation ◽  
Tight Junction ◽  
Sertoli Cell ◽  
Germ Cells ◽  
Sertoli Cells ◽  
Proliferative Activity ◽  
Terminal Differentiation ◽  
Tight Junction Proteins ◽  
Junction Proteins ◽  
Blood Testis Barrier

The concept of terminal differentiation of Sertoli cells has been challenged and this new information has important implications for male fertility. The mammalian Sertoli cell has two distinct functions: (i) formation of the seminiferous cords and (ii) provision of nutritional and structural support to the developing germ cells. For these to occur successfully, Sertoli cells must undergo numerous maturational changes between foetal and adult life, the main switches occur around the onset of puberty, coincident with the rise in serum gonadotrophins. These switches include the loss of proliferative activity and the formation of the blood testis barrier. Follicle stimulating hormone (FSH) plays a key role in supporting Sertoli cell proliferation in early postnatal life and thus is critical in establishing sperm output in adulthood. After puberty, the size of the Sertoli cell population is considered to be stable and unmodifiable by hormones. This accepted view has been contested as data shows that the size of the adult Sertoli cell population is modifiable by hormone suppression, and that Sertoli cells can regain proliferative activity when stimulated by FSH in the Djungarian hamster1. The molecular mechanism(s) by which Sertoli cells re-enter proliferation are not known in this model however a study demonstrated that helix-loop-inhibitor of differentiation proteins can induce terminally differentiated Sertoli cells to re-enter the cell cycle and proliferate2. Thyroid hormone and testosterone may be involved in the cessation of Sertoli cell proliferation. Gonadotrophin suppression in the adult Djungarian hamster also results in the disruption of the blood testis barrier and spatial organisation of the inter Sertoli cell tight junction proteins and as a consequence the loss of all germ cells that reside inside the blood testis barrier. FSH restores the organisation of these tight junction proteins, which is associated with the appearance of more mature germ cells. It is expected that the integrity of the blood testis barrier is also re-established. It is suggested that this demonstrated plasticity of the adult Sertoli cell may be relevant in clinical settings, particularly to some types of infertility and testicular malignancies where Sertoli cells have failed to undergo these important maturational switches. (1)Chaudhary et al. (2005) Biol. Reprod. 72, 1205. (2)Meachem et al. (2005) Biol. Reprod. 72, 1187.

scholarly journals Regulation of testicular tight junctions by gonadotrophins in the adult Djungarian hamster in vivo

Reproduction ◽  
2008 ◽  
Vol 135 (6) ◽  
pp. 867-877 ◽  
Author(s):  
Gerard A Tarulli ◽  
Sarah J Meachem ◽  
Stefan Schlatt ◽  
Peter G Stanton
Keyword(s):  
Tight Junction ◽  
Adaptor Protein ◽  
Tight Junction Protein ◽  
Mrna Levels ◽  
Tight Junction Proteins ◽  
Djungarian Hamster ◽  
Junction Protein ◽  
Protein Localisation ◽  
Junction Proteins

This study aimed to assess the effect of gonadotrophin suppression and FSH replacement on testicular tight junction dynamics and blood–testis barrier (BTB) organisation in vivo, utilising the seasonal breeding Djungarian hamster. Confocal immunohistology was used to assess the cellular organisation of tight junction proteins and real-time PCR to quantify tight junction mRNA. The effect of tight junction protein organisation on the BTB permeability was also investigated using a biotin-linked tracer. Tight junction protein (claudin-3, junctional adhesion molecule (JAM)-A and occludin) localisation was present but disorganised after gonadotrophin suppression, while mRNA levels (claudin-11, claudin-3 and occludin) were significantly (two- to threefold) increased. By contrast, both protein localisation and mRNA levels for the adaptor protein zona occludens-1 decreased after gonadotrophin suppression. FSH replacement induced a rapid reorganisation of tight junction protein localisation. The functionality of the BTB (as inferred by biotin tracer permeation) was found to be strongly associated with the organisation and localisation of claudin-11. Surprisingly, JAM-A was also recognised on spermatogonia, suggesting an additional novel role for this protein in trans-epithelial migration of germ cells across the BTB. It is concluded that gonadotrophin regulation of tight junction proteins forming the BTB occurs primarily at the level of protein organisation and not gene transcription in this species, and that immunolocalisation of the organised tight junction protein claudin-11 correlates with BTB functionality.

Role of AMPK in the expression of tight junction proteins in heat-treated porcine Sertoli cells

2018 ◽  
Vol 121 ◽  
pp. 42-52 ◽  
Author(s):  
Wei-Rong Yang ◽  
Ting-Ting Liao ◽  
Zi-Qiang Bao ◽  
Cai-Quan Zhou ◽  
Hong-Yan Luo ◽  
...  
Keyword(s):  
Tight Junction ◽  
Sertoli Cells ◽  
Tight Junction Proteins ◽  
Heat Treated ◽  
Junction Proteins

Intestinal epithelial cell proliferation, apoptosis and expression of tight junction proteins in patients with obstructive jaundice

2010 ◽  
Vol 41 (2) ◽  
pp. 117-125 ◽  
Author(s):  
Stelios F. Assimakopoulos ◽  
Athanassios C. Tsamandas ◽  
Emanuel Louvros ◽  
Constantine E. Vagianos ◽  
Vassiliki N. Nikolopoulou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Obstructive Jaundice ◽  
Tight Junction ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Epithelial Cell Proliferation ◽  
Tight Junction Proteins ◽  
Junction Proteins

scholarly journals A Major Lung CD103 (αE)-β7 Integrin-Positive Epithelial Dendritic Cell Population Expressing Langerin and Tight Junction Proteins

2006 ◽  
Vol 176 (4) ◽  
pp. 2161-2172 ◽  
Author(s):  
Sun-Sang J. Sung ◽  
Shu Man Fu ◽  
C. Edward Rose ◽  
Felicia Gaskin ◽  
Shyr-Te Ju ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Tight Junction ◽  
Cell Population ◽  
Tight Junction Proteins ◽  
Dendritic Cell Population ◽  
Junction Proteins

scholarly journals Metformin counteracts the effects of FSH on rat Sertoli cell proliferation

Reproduction ◽  
2018 ◽  
Vol 156 (2) ◽  
pp. 93-101 ◽  
Author(s):  
Gustavo Marcelo Rindone ◽  
Agostina Gorga ◽  
Mariana Regueira ◽  
Eliana Herminia Pellizzari ◽  
Selva Beatriz Cigorraga ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Sertoli Cell ◽  
Sertoli Cells ◽  
Molecular Mechanisms ◽  
Pediatric Population ◽  
Follicle Stimulating Hormone ◽  
Acetyl Coa Carboxylase ◽  
Cell Cycle Inhibitor ◽  
Cell Mitogen

Metformin (MET) is one of the most widely used anti-hyperglycemic agents for treating patients with type 2 diabetes and it has started to be used in pediatric population at ages when Sertoli cells are still proliferating. It is well known that follicle-stimulating hormone (FSH) is the major Sertoli cell mitogen. The aim of the study is to investigate a possible effect of MET, which has been shown to have anti-proliferative properties, on FSH regulation of postnatal Sertoli cell proliferation and on the molecular mechanisms involved in this regulation. The present study was performed in eight-day-old rat Sertoli cell cultures. The results obtained show that MET in the presence of FSH increases phosphorylated acetyl-CoA carboxylase and decreases phosphorylated p70S6K levels. Moreover, we show that MET decreases FSH-stimulated Sertoli cell proliferation, and this decrease is accompanied by a reduction in FSH-stimulated Ccnd1 and Ccnd2 expression and an increase in cell cycle inhibitor p21Cip expression. Altogether, these results suggest that MET can, at least in part, counteract the effect of FSH on postnatal Sertoli cell proliferation.

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