Localization of EFA6 (exchange factor for ARF6) isoform D in steroidogenic testicular Leydig cells of adult mice

2018 ◽  
Vol 120 (3) ◽  
pp. 263-268
Author(s):  
Surang Chomphoo ◽  
Sawetree Pakkarato ◽  
Tarinee Sawatpanich ◽  
Hiroyuki Sakagami ◽  
Hisatake Kondo ◽  
...  
Keyword(s):  
Leydig Cells ◽  
Exchange Factor ◽  
Adult Mice

Gonadal expression of c-kit encoded at the W locus of the mouse

Development ◽  
1990 ◽  
Vol 110 (4) ◽  
pp. 1057-1069 ◽  
Author(s):  
K. Manova ◽  
K. Nocka ◽  
P. Besmer ◽  
R.F. Bachvarova
Keyword(s):  
In Situ Hybridization ◽  
Germ Cells ◽  
Leydig Cells ◽  
Interstitial Tissue ◽  
Type B ◽  
Age Dependence ◽  
Oocyte Growth ◽  
Adult Mice

Recently, it has been shown that the c-kit proto-oncogene is encoded at the white spotting (W) locus in mice. Mutations of this gene cause depletion of germ cells, some hematopoietic cells and melanocytes. In order to define further the role of c-kit in gametogenesis, we have examined its expression in late fetal and postnatal ovaries and in postnatal testis. By RNA blot analysis, c-kit transcripts were not detected in late fetal ovaries but appeared at birth. The relative amount reached a maximum in ovaries of juvenile mice, and decreased in adult ovaries. c-kit transcripts were present in increasing amounts in isolated primordial, growing and full-grown oocytes, as well as in ovulated eggs. Little was detected in early 2-cell embryos and none in blastocysts. In situ hybridization revealed c-kit transcripts in a few oocytes of late fetal ovaries and in all oocytes (from primordial to full-grown) in ovaries from juvenile and adult mice. Expression was also observed in ovarian interstitial tissue from 14 days of age onward. Using indirect immunofluorescence, the c-kit protein was detected on the surface of primordial, growing and full-grown oocytes, as well as on embryos at the 1- and 2-cell stages; little remained in blastocysts. In situ hybridization analysis of testes from mice of different ages demonstrated expression in spermatogonia from 6 days of age onward. Using information provided by determining the stage of the cycle of the seminiferous epithelium for a given tubule and by following the age dependence of labeling, it was concluded that the period of expression of c-kit extends from at least as early as type A2 spermatogonia through type B spermatogonia and into preleptotene spermatocytes. Leydig cells were labelled at all ages examined. The expression pattern in oocytes correlates most strongly with oocyte growth and in male germ cells with gonial proliferation.

scholarly journals Neuregulin 1 Regulates Proliferation of Leydig Cells to Support Spermatogenesis and Sexual Behavior in Adult Mice

Endocrinology ◽  
2016 ◽  
Vol 157 (12) ◽  
pp. 4899-4913 ◽  
Author(s):  
Takashi Umehara ◽  
Ikko Kawashima ◽  
Tomoko Kawai ◽  
Yumi Hoshino ◽  
Ken-ichirou Morohashi ◽  
...  
Keyword(s):  
Sexual Behavior ◽  
Leydig Cells ◽  
Neuregulin 1 ◽  
Adult Mice

scholarly journals Role of gonadotrophins in regulating numbers of Leydig and Sertoli cells during fetal and postnatal development in mice

Reproduction ◽  
2001 ◽  
pp. 227-234 ◽  
Author(s):  
PJ Baker ◽  
PJ O'Shaughnessy
Keyword(s):  
Cell Volume ◽  
Postnatal Development ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Normal Values ◽  
Fold Increase ◽  
Adult Mice ◽  
Number Of Cells

The role of the gonadotrophins in regulating numbers of Leydig and Sertoli cells during fetal and postnatal development was examined using normal mice and hypogonadal (hpg) mice, which lack circulating gonadotrophins. The disector method was used to determine the number of cells from day 16 of gestation until adulthood. The numbers of Leydig cells did not change significantly between day 16 of gestation and day 5 after parturition in normal mice and were not significantly different from numbers in hpg mice at any age up to day 5 after parturition. There was a 16-fold increase in the number of Leydig cells in normal mice between day 5 and day 20 after parturition, followed by a further doubling of number of cells between day 20 and adulthood. The number of Leydig cells in hpg testes did not change between day 5 and day 20 after parturition but doubled between day 20 and adulthood so that the number of cells was about 10% of normal values from day 20 onwards. Leydig cell volume was constant in normal animals from birth up to day 20 and then showed a 2.5-fold increase in adult animals. Leydig cell volume was normal in hpg testes at birth but decreased thereafter and was about 20% of normal volume in adult mice. The number of Sertoli cells increased continuously from day 16 of gestation to day 20 after gestation in normal mice and then remained static until adulthood. The number of Sertoli cells in hpg testes was normal throughout fetal life but was reduced by about 30% on day 1 (day of parturition). Thereafter, Sertoli cells proliferated at a slower rate but over a longer period in the hpg testis so that on day 20 after parturition the number of Sertoli cells was about 50% of normal values, whereas in adult mice the number was 65% of normal. The number of gonocytes did not change between day 16 of gestation and day 1 and did not differ between normal and hpg testes. The number of gonocytes increased nine-fold in normal testes but only three-fold in hpg testes between day 1 and day 5 after parturition. Gonocytes differentiated into spermatogonia in both normal and hpg testes between day 5 and day 20 after parturition. These results show: (i) that fetal development of both Sertoli and Leydig cells is independent of gonadotrophins; (ii) that normal differentiation and proliferation of the adult Leydig cell population (starting about day 10 after parturition) is dependent on the presence of gonadotrophins; and (iii) that the number of Sertoli cells after birth is regulated by gonadotrophins, although proliferation will continue, at a lower rate and for longer, in the absence of gonadotrophins.

scholarly journals Dickkopf-Like1 Regulates Postpubertal Spermatocyte Apoptosis and Testosterone Production

Endocrinology ◽  
2008 ◽  
Vol 150 (1) ◽  
pp. 404-412 ◽  
Author(s):  
Olga Dakhova ◽  
Diana O'Day ◽  
Noe Kinet ◽  
Nur Yucer ◽  
Mary Wiese ◽  
...  
Keyword(s):  
Leydig Cells ◽  
Fas Ligand ◽  
Sperm Count ◽  
Negative Regulator ◽  
Steroidogenic Factor 1 ◽  
Adult Testis ◽  
Adult Mice ◽  
Sperm Counts ◽  
Apoptotic Activity ◽  
The One

Dickkopf-like1 (Dkkl1) encodes a glycoprotein secreted by postmeiotic male germ cells. We report here that adult Dkkl1-deficient males have elevated sperm counts caused by a decrease in postpubertal spermatocyte apoptosis and display, upon aging, increased local production of testosterone. Molecular analyses identified the Fas death ligand (FasL) as a target for Dkkl1 pro-apoptotic activity in adult mice. Accordingly, adult FasL-deficient gld mice display an increased sperm count and decreased spermatocyte apoptosis phenotype similar to the one observed in Dkkl1-deficient mice. We also show that the elevated testosterone level observed in aging Dkkl1-deficient males is secondary to increased expression in Leydig cells of CYP11A and CYP17, two genes implicated in steroidogenesis. Furthermore, treatment of Leydig cells with Dkkl1 decreases DNA binding and transcriptional activity of steroidogenic factor 1, a pivotal regulator of gene expression in testis. Thus, this study establishes Dkkl1 as a negative regulator of adult testis homeostasis and identifies a novel, Dkkl1/FasL-dependent, regulation that specifically controls the number of postpubertal spermatocytes. Dickkopf-like 1 negatively regulates adult testis biology by promoting spermatocyte apoptosis via Fas ligand activation and by limiting testosterone synthesis in Leydig cells.

Morphometric analysis of testicular Leydig cells in normal adult mice

1982 ◽  
Vol 204 (4) ◽  
pp. 333-339 ◽  
Author(s):  
H. Mori ◽  
D. Shimizu ◽  
R. Fukunishi ◽  
A. Kent Christensen
Keyword(s):  
Morphometric Analysis ◽  
Leydig Cells ◽  
Normal Adult ◽  
Adult Mice

scholarly journals Wt1 dictates the fate of fetal and adult Leydig cells during development in the mouse testis

2014 ◽  
Vol 307 (12) ◽  
pp. E1131-E1143 ◽  
Author(s):  
Qing Wen ◽  
Qiao-Song Zheng ◽  
Xi-Xia Li ◽  
Zhao-Yuan Hu ◽  
Fei Gao ◽  
...  
Keyword(s):  
Leydig Cell ◽  
Testosterone Level ◽  
Leydig Cells ◽  
Wilms Tumor ◽  
Suppressor Gene ◽  
Testicular Development ◽  
Gene Encoding ◽  
Testis Development ◽  
Adult Mice ◽  
Serum Lh

Wilms' tumor 1 ( Wt1) is a tumor suppressor gene encoding ∼24 zinc finger transcription factors. In the mammalian testis, Wt1 is expressed mostly by Sertoli cells (SCs) involved in testis development, spermatogenesis, and adult Leydig cell (ALC) steroidogenesis. Global knockout (KO) of Wt1 is lethal in mice due to defects in embryogenesis. Herein, we showed that Wt1 is involved in regulating fetal Leydig cell (FLC) degeneration and ALC differentiation during testicular development. Using Wt1−/flox; Amh-Cre mice that specifically deleted Wt1 in the SC vs. age-matched wild-type (WT) controls, FLC-like-clusters were found in Wt1-deficient testes that remained mitotically active from postnatal day 1 (P1) to P56, and no ALC was detected at these ages. Leydig cells in mutant adult testes displayed morphological features of FLC. Also, FLC-like cells in adult mutant testes had reduced expression in ALC-associated genes Ptgds, Sult1e1, Vcam1, Hsd11b1, Hsd3b6, and Hsd17b3 but high expression of FLC-associated genes Thbs2 and Hsd3b1. Whereas serum LH and testosterone level in mutant mice were not different from controls, intratesticular testosterone level was significantly reduced. Deletion of Wt1 gene also perturbed the expression of steroidogenic enzymes Star, P450c17, Hsd3b6, Hsd3b1, Hsd17b1, and Hsd17b3. FLCs in adult mutant testes failed to convert androstenedione to testosterone due to a lack of Hsd17b3, and this defect was rescued by coculturing with fetal SCs. In summary, FLC-like cells in mutant testes are putative FLCs that remain mitotically active in adult mice, illustrating that Wt1 dictates the fate of FLC and ALC during postnatal testis development.

scholarly journals Effect of Phitofert® on testicular function of vasectomized mature mice

2018 ◽  
Vol 11 (2) ◽  
pp. 9-16
Author(s):  
Muna Yousif ◽  
saad Al-Dujal ◽  
Jawad Arrak
Keyword(s):  
Dna Fragmentation ◽  
Adult Male ◽  
Leydig Cells ◽  
Treated Group ◽  
Reproductive Hormones ◽  
Current Data ◽  
Seminiferous Tubules ◽  
Control Group ◽  
Adult Mice ◽  
Serum Lh

This study was designed to evaluate the role of Phitofert® in the improvement of testes function and attenuating DNA fragmentation in vasectomized and healthy adult mice. Twenty four adult male breed such Albino mice were randomly and equally divided into four groups (G1, G2, G3 and G4). Mice were treated for 35days as follows: the G1 mice were non-vasectomized and given DW and served as controls, mice in G2 were non-vasectomized and given Phitofert® daily with a dose of 0.035mg/kg BW, mice in G3 were vasectomized without treatment while the mice in G4 were vasectomized and given same dose of Phitofert®. At the end of the experiment, fasting blood samples were collected by cardiac puncture for measuring LH and FSH hormones concentrations and section from testes were taken tomeasure the number of Leydig cells and diameter of semniferous tubules. The results of current data showed significant increase of serum LH and FSH concentrations in G2 healthy treated group as compared with control and other groups. Also, the treatment of G4 vasectomized mice with Phitofert® caused significant increase in serum concentration of the above hormones as compared with G3 vasectomized non-treated. The study showed that DNA fragmentation that resulted from the G2 healthy treated mice were lower than that obtained from the control group and other vasectomized mice (G3, G4). The diameters of the seminiferous tubules and the numbers of Leydig cells showed significant increase in healthy and vasectomized treated group (G1, G4) as compared with G3 vasectomized non-treated group. It was concluded that healthy and vasectomized treated of adult male mice with Phitofert® lead to clear improvement of level of reproductive hormones.

Binucleate Spermiogenesis in the Mouse

1972 ◽  
Vol 30 ◽  
pp. 112-113
Author(s):  
John J. Wolosewick
Keyword(s):  
Electron Microscopy ◽  
Phosphate Buffer ◽  
Seminiferous Epithelium ◽  
Mouse Testis ◽  
Germinal Epithelium ◽  
Intercellular Bridges ◽  
Adult Mice ◽  
Cervical Dislocation ◽  
Human And Mouse

Classically, the male germinal epithelium is depicted as synchronously developing uninucleate spermatids conjoined by intercellular bridges. Recently, binucleate and multinucleate spermatids from human and mouse testis have been reported. The present paper describes certain developmental events in one type of binucleate spermatid in the seminiferous epithelium of the mouse.Testes of adult mice (ABP Jax) were removed from the animals after cervical dislocation and placed into 2.5% glutaraldehyde/Millonig's phosphate buffer (pH 7.2). Testicular capsules were gently split and separated, exposing the tubules. After 15 minutes the tissue was carefully cut into cubes (approx. 1mm), fixed for an additional 45 minutes and processed for electron microscopy.

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