scholarly journals Leydig cell genes change their expression and association with polysomes in a stage-specific manner in the adult mouse testis†,‡

2018 ◽  
Vol 98 (5) ◽  
pp. 722-738 ◽  
Author(s):  
Estela J Jauregui ◽  
Debra Mitchell ◽  
Savanna M Garza ◽  
Traci Topping ◽  
Cathryn A Hogarth ◽  
...  
Keyword(s):  
Germ Cell ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Adult Mouse ◽  
Cell Function ◽  
Cell Development ◽  
Seminiferous Epithelium ◽  
Mouse Testis ◽  
Germ Cell Development ◽  
Specific Manner

Abstract Spermatogenesis in mammals occurs in a very highly organized manner within the seminiferous epithelium regulated by different cell types in the testis. Testosterone produced by Leydig cells regulates blood–testis barrier formation, meiosis, spermiogenesis, and spermiation. However, it is unknown whether Leydig cell function changes with the different stages of the seminiferous epithelium. This study utilized the WIN 18,446 and retinoic acid (RA) treatment regime combined with the RiboTag mouse methodology to synchronize male germ cell development and allow for the in vivo mapping of the Leydig cell translatome across the different stages of one cycle of the seminiferous epithelium. Using microarrays analysis, we identified 11 Leydig cell-enriched genes that were expressed in stage-specific manner such as the glucocorticoid synthesis and transport genes, Cyp21a1 and Serpina6. In addition, there were nine Leydig cell transcripts that change their association with polysomes in correlation with the different stages of the spermatogenic cycle including Egr1. Interestingly, the signal intensity of EGR1 and CYP21 varied among Leydig cells in the adult asynchronous testis. However, testosterone levels across the different stages of germ cell development did not cycle. These data show, for the first time, that Leydig cell gene expression changes in a stage-specific manner during the cycle of the seminiferous epithelium and indicate that a heterogeneous Leydig cell population exists in the adult mouse testis.

scholarly journals Effects of environmental Bisphenol A exposures on germ cell development and Leydig cell function in the human fetal testis

PLoS ONE ◽  
2018 ◽  
Vol 13 (1) ◽  
pp. e0191934 ◽  
Author(s):  
Soria Eladak ◽  
Delphine Moison ◽  
Marie-Justine Guerquin ◽  
Gabriele Matilionyte ◽  
Karen Kilcoyne ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Germ Cell ◽  
Leydig Cell ◽  
Cell Function ◽  
Cell Development ◽  
Germ Cell Development ◽  
Fetal Testis ◽  
Leydig Cell Function

scholarly journals The Pluripotency-Associated Gene Dppa4 Is Dispensable for Embryonic Stem Cell Identity and Germ Cell Development but Essential for Embryogenesis

2009 ◽  
Vol 29 (11) ◽  
pp. 3186-3203 ◽  
Author(s):  
Babita Madan ◽  
Vikas Madan ◽  
Odile Weber ◽  
Philippe Tropel ◽  
Carmen Blum ◽  
...  
Keyword(s):  
Germ Cell ◽  
Cell Function ◽  
Es Cells ◽  
Embryonic Stem ◽  
Cell Development ◽  
Es Cell ◽  
Pluripotent Cells ◽  
Cell Identity ◽  
Germ Cell Development ◽  
Skeletal Defects

ABSTRACT Dppa4 (developmental pluripotency-associated 4) has been identified in several high-profile screens as a gene that is expressed exclusively in pluripotent cells. It encodes a nuclear protein with an SAP-like domain and appears to be associated preferentially with transcriptionally active chromatin. Its exquisite expression pattern and results of RNA interference experiments have led to speculation that Dppa4, as well as its nearby homolog Dppa2, might play essential roles in embryonic stem (ES) cell function and/or germ cell development. To rigorously assess suggested roles, we have generated Dppa4-deficient and Dppa4/Dppa2 doubly deficient ES cells, as well as mice lacking Dppa4. Contrary to predictions, we find that Dppa4 is completely dispensable for ES cell identity and germ cell development. Instead, loss of Dppa4 in mice results in late embryonic/perinatal death and striking skeletal defects with partial penetrance. Thus, surprisingly, Dppa4-deficiency affects tissues that apparently never transcribed the gene, and at least some loss-of-function defects manifest phenotypically at an embryonic stage long after physiologic Dppa4 expression has ceased. Concomitant with targeted gene inactivation, we have introduced into the Dppa4 locus a red fluorescent marker (tandem-dimer red fluorescent protein) that is compatible with green fluorescent proteins and allows noninvasive visualization of pluripotent cells and reprogramming events.

scholarly journals Slit/Robo signaling regulates Leydig cell steroidogenesis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Emmanuelle Martinot ◽  
Derek Boerboom
Keyword(s):  
Cancer Progression ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Adult Mouse ◽  
Primary Cultures ◽  
Mouse Testis ◽  
Mrna Levels ◽  
Pathologic Processes ◽  
In Vitro Treatment

Abstract Background First identified as a regulator of neuronal axon guidance, Slit/Robo signaling has since been implicated in additional physiologic and pathologic processes, such as angiogenesis, organogenesis and cancer progression. However, its roles in the regulation of testis function have been little explored. Methods Immunohistochemistry and RT-qPCR analyses were performed to detect the expression of Slit/Robo signaling effectors in the adult mouse testis. To identify the roles and mechanisms of Slit/Robo signaling in the regulation of steroidogenesis, RT-qPCR, immunoblotting and hormone measurements were carried out using Leydig cells (primary cultures and the MA10 cell line) treated with exogenous SLIT ligands, and testes from Robo1-null mice. Results Slit1, -2 and -3 and Robo1 and -2 expression was detected in the adult mouse testis, particularly in Leydig cells. In vitro treatment of Leydig cells with exogenous SLIT ligands led to a decrease in the expression of the steroidogenic genes Star, Cyp11a1, and Cyp17a1. SLIT2 treatment decreased the phosphorylation of the key steroidogenic gene regulator CREB, possibly in part by suppressing AKT activity. Furthermore, SLIT2 treatment reduced the responsiveness of MA10 cells to luteinizing hormone by decreasing the expression of Lhcgr. Consistent with these in vitro results, an increase in testicular Star mRNA levels and intra-testicular testosterone concentrations were found in Robo1-null mice. Finally, we showed that the expression of the Slit and Robo genes in Leydig cells is enhanced by testosterone treatment in vitro, by an AR-independent mechanism. Conclusion Taken together, these results suggest that Slit/Robo signaling represents a novel mechanism that regulates Leydig cell steroidogenesis. It may act in an autocrine/paracrine manner to mediate negative feedback by testosterone on its own synthesis.

The germ cell development strategy and seasonal changes in spermatogenesis and Leydig cell morphologies of the spiny lizard Sceloporus mucronatus (Squamata: Phrynosomatidae)

Zoomorphology ◽  
2013 ◽  
Vol 133 (2) ◽  
pp. 151-165 ◽  
Author(s):  
Maricela Villagrán-SantaCruz ◽  
Ma. Juana Hernández-Aguacaliente ◽  
Fausto R. Méndez-de la Cruz ◽  
Kevin M. Gribbins ◽  
Gisela Granados-González ◽  
...  
Keyword(s):  
Germ Cell ◽  
Development Strategy ◽  
Leydig Cell ◽  
Seasonal Changes ◽  
Cell Development ◽  
Germ Cell Development

scholarly journals Impaired Leydig Cell Function in Infertile Men: A Study of 357 Idiopathic Infertile Men and 318 Proven Fertile Controls

2004 ◽  
Vol 89 (7) ◽  
pp. 3161-3167 ◽  
Author(s):  
A.-M. Andersson ◽  
N. Jørgensen ◽  
L. Frydelund-Larsen ◽  
E. Rajpert-De Meyts ◽  
N. E. Skakkebæk
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Infant Development ◽  
Cell Function ◽  
Serum Testosterone ◽  
Seminiferous Epithelium ◽  
Lower Serum ◽  
Infertile Men ◽  
Serum Lh ◽  
Leydig Cell Function

Abstract To investigate whether an impaired Leydig cell function is present in severely oligospermic men, serum testosterone (T), LH, estradiol (E2), and SHBG levels in 357 idiopathic infertile men were compared with levels in 318 proven fertile men. In addition, the T/LH ratio, E2/T ratio, and calculated free T index (cFT) were compared between the two groups. A shift toward lower serum T levels, cFT, and T/LH ratio and higher serum LH, E2, and E2/T levels was observed in the group of infertile men. On average, the infertile men had 18, 26, and 34% lower serum T, cFT, and T/LH levels, respectively, and 19, 18, and 33% higher serum LH, E2, and E2/T levels, respectively, than the fertile men. Twelve percent of the infertile men had a serum T level that fell below the 2.5 percentile of the fertile levels, and 15% of the infertile men had a LH level that was above the 97.5 percentile of the fertile levels. Thus, the group of infertile men showed significant signs of impaired Leydig cell function in parallel to their impaired spermatogenesis. The association of decreased spermatogenesis and impaired Leydig cell function might reflect a disturbed paracrine communication between the seminiferous epithelium and the Leydig cells, triggered by distorted function of the seminiferous epithelium. On the other hand, the parallel impairment of spermatogenesis and Leydig cells may reflect a congenital dysfunction of both compartments caused by a testicular dysgenesis during fetal/infant development.

scholarly journals Multiplex shRNA Screening of Germ Cell Development by in Vivo Transfection of Mouse Testis

2016 ◽  
Vol 7 (1) ◽  
pp. 247-255 ◽  
Author(s):  
Nicholas R. Y. Ho ◽  
Abul R. Usmani ◽  
Yan Yin ◽  
Liang Ma ◽  
Donald F. Conrad
Keyword(s):  
Germ Cell ◽  
Cell Development ◽  
Mouse Testis ◽  
Germ Cell Development ◽  
In Vivo Transfection

APPLICATION OF MICROPIXE TO ELEMENTAL IMAGING OF THE RAT TESTIS

2001 ◽  
Vol 11 (03n04) ◽  
pp. 103-110 ◽  
Author(s):  
S. HOMMA-TAKEDA ◽  
Y. NISHIMURA ◽  
Y. WATANABE ◽  
H. IMASEKI ◽  
M. YUKAWA
Keyword(s):  
Trace Elements ◽  
Germ Cell ◽  
Cell Development ◽  
Seminiferous Epithelium ◽  
Thick Section ◽  
Cell Type ◽  
Germ Cell Development ◽  
Elemental Imaging ◽  
Rat Testis ◽  
Powerful Technique

The MicroPIXE technique was employed to reveal detailed distributions of trace elements in the testis, which distinguish the cell type-differences corresponding to the germ cell development (the 14 designated stages of the seminiferous epithelium cycle). Clear elemental imagings were obtained for P and S with a 50 μ m-thick section; S was higher in elongated spermatids in stages VII-VII, where a lower level of P was observed. Elemental imagings of Cu, Fe, Mn, Se, and Zn were obscure compared with P and S, but information about their localization in the seminiferous epithelium was obtained. These results suggest that microPIXE analysis is a powerful technique for investigation of elemental dynamics in the testis, although an improvement of detection for testicular trace elements is required.

scholarly journals Male 41, XXY* Mice as a Model for Klinefelter Syndrome: Hyperactivation of Leydig Cells

Endocrinology ◽  
2010 ◽  
Vol 151 (6) ◽  
pp. 2898-2910 ◽  
Author(s):  
Joachim Wistuba ◽  
C. Marc Luetjens ◽  
Jan-Bernd Stukenborg ◽  
Andreas Poplinski ◽  
Steffi Werler ◽  
...  
Keyword(s):  
Germ Cell ◽  
X Chromosome ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Klinefelter Syndrome ◽  
Cell Loss ◽  
Endocrine Function ◽  
Maximal Response ◽  
Different Ages

Sex chromosome imbalance in males is linked to a supernumerary X chromosome, a condition resulting in Klinefelter syndrome (KS; 47, XXY). KS patients suffer from infertility, hypergonadotropic hypogonadism, and cognitive impairments. Mechanisms of KS pathophysiology are poorly understood and require further exploration using animal models. Therefore, we phenotypically characterized 41, XXY* mice of different ages, evaluated observed germ cell loss, studied X-inactivation, and focused on the previously postulated impaired Leydig cell maturation and function as a possible cause of the underandrogenization seen in KS. Xist methylation analysis revealed normal X-chromosome inactivation similar to that seen in females. Germ cell loss was found to be complete and to occur during the peripubertal phase. Significantly elevated FSH and LH levels were persistent in 41, XXY* mice of different ages. Although Leydig cell hyperplasia was prominent, isolated XXY* Leydig cells showed a mature mRNA expression profile and a significantly higher transcriptional activity compared with controls. Stimulation of XXY* Leydig cells in vitro by human chorionic gonadotropin indicated a mature LH receptor whose maximal response exceeded that of control Leydig cells. The hyperactivity of Leydig cells seen in XXY* mice suggests that the changes in the endocrine milieu observed in KS is not due to impaired Leydig cell function. We suggest that the embedding of Leydig cells into the changed testicular environment in 41 XXY* males as such influences their endocrine function.

scholarly journals Sgpl1 deletion elevates S1P levels, contributing to NPR2 inactivity and p21 expression that block germ cell development

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Feifei Yuan ◽  
Zhijuan Wang ◽  
Yanli Sun ◽  
Hongwei Wei ◽  
Yanying Cui ◽  
...  
Keyword(s):  
Germ Cell ◽  
Granulosa Cells ◽  
Leydig Cells ◽  
Kinase Inhibitor ◽  
Cell Development ◽  
Cyclin Dependent Kinase ◽  
Follicle Growth ◽  
Germ Cell Development ◽  
Cyclin Dependent Kinase Inhibitor ◽  
Sphingosine 1 Phosphate

AbstractSphingosine phosphate lyase 1 (SGPL1) is a highly conserved enzyme that irreversibly degrades sphingosine-1-phosphate (S1P). Sgpl1-knockout mice fail to develop germ cells, resulting in infertility. However, the molecular mechanism remains unclear. The results of the present study showed that SGPL1 was expressed mainly in granulosa cells, Leydig cells, spermatocytes, and round spermatids. Sgpl1 deletion led to S1P accumulation in the gonads. In the ovary, S1P decreased natriuretic peptide receptor 2 (NPR2) activity in granulosa cells and inhibited early follicle growth. In the testis, S1P increased the levels of cyclin-dependent kinase inhibitor 1A (p21) and apoptosis in Leydig cells, thus resulting in spermatogenesis arrest. These results indicate that Sgpl1 deletion increases intracellular S1P levels, resulting in the arrest of female and male germ cell development via different signaling pathways.

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