Interdependence of Platelet-Derived Growth Factor and Estrogen-Signaling Pathways in Inducing Neonatal Rat Testicular Gonocytes Proliferation1

Thuillier, Raphaël; Mazer, Monty; Manku, Gurpreet; Boisvert, Annie; Wang, Yan; Culty, Martine

doi:10.1095/biolreprod.109.081729

Cited by 54 publications

(54 citation statements)

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“…However, in the same study, RA was reported to slightly increase PND3 gonocyte numbers and have no effect on apoptosis. Moreover, activin A and androgen were reported to be negative regulators of fetal gonocyte proliferation, whereas we did not find any effect of testosterone on PND3 gonocyte proliferation in vitro (Merlet et al 2007, Thuillier et al 2010, Mendis et al 2011.…”

Section: Introductioncontrasting

confidence: 90%

“…This transdifferentiation requires activation of the ERK1/2 and Smad2/3 signaling pathways (Zhang et al 2013b). Interestingly, we have previously shown that ERK1/2 activation is necessary for gonocyte proliferation, but that it does not participate in gonocyte differentiation R148 G Manku and M Culty (Thuillier et al 2010, Manku et al 2014. The ability of SSCs to transdifferentiate into mature hepatocytes is quite remarkable, illustrating the high plasticity of these unipotent stem cells, capable of reverting to pluripotency under specific conditions, representing potential clinical use in the treatment of liver diseases (Zhang et al 2013b).…”

Section: Ra-induced Decreases In Mirc1 and Mirc3 In Thy1mentioning

confidence: 99%

“…One common characteristic of fetal and postnatal gonocytes is that they are the site of intense DNA remethylation, required for the acquisition of paternal imprints and transposon silencing (Trasler 2009). While platelet-derived growth factor-BB (PDGF-BB) and 17b-estradiol were shown to induce neonatal gonocyte proliferation via MAPK activation (Li et al 1997, Basciani et al 2008, Thuillier et al 2010, the factors inducing fetal gonocyte proliferation have not been fully identified. The difference between mitotic fetal and neonatal rat gonocytes was clearly illustrated by their different responses to all-trans retinoic acid (RA) in organ culture studies.…”

Section: Introductionmentioning

confidence: 99%

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Mammalian gonocyte and spermatogonia differentiation: recent advances and remaining challenges

Manku¹,

Culty²

2015

Reproduction

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127

105

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The production of spermatozoa relies on a pool of spermatogonial stem cells (SSCs), formed in infancy from the differentiation of their precursor cells, the gonocytes. Throughout adult life, SSCs will either self-renew or differentiate, in order to maintain a stem cell reserve while providing cells to the spermatogenic cycle. By contrast, gonocytes represent a transient and finite phase of development leading to the formation of SSCs or spermatogonia of the first spermatogenic wave. Gonocyte development involves phases of quiescence, cell proliferation, migration, and differentiation. Spermatogonia, on the other hand, remain located at the basement membrane of the seminiferous tubules throughout their successive phases of proliferation and differentiation. Apoptosis is an integral part of both developmental phases, allowing for the removal of defective cells and the maintenance of proper germ-Sertoli cell ratios. While gonocytes and spermatogonia mitosis are regulated by distinct factors, they both undergo differentiation in response to retinoic acid. In contrast to postpubertal spermatogenesis, the early steps of germ cell development have only recently attracted attention, unveiling genes and pathways regulating SSC self-renewal and proliferation. Yet, less is known on the mechanisms regulating differentiation. The processes leading from gonocytes to spermatogonia have been seldom investigated. While the formation of abnormal gonocytes or SSCs could lead to infertility, defective gonocyte differentiation might be at the origin of testicular germ cell tumors. Thus, it is important to better understand the molecular mechanisms regulating these processes. This review summarizes and compares the present knowledge on the mechanisms regulating mammalian gonocyte and spermatogonial differentiation.

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Section: Introductioncontrasting

confidence: 90%

Section: Ra-induced Decreases In Mirc1 and Mirc3 In Thy1mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mammalian gonocyte and spermatogonia differentiation: recent advances and remaining challenges

Manku¹,

Culty²

2015

Reproduction

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127

105

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“…However, their direct influence cannot be ruled out and this has been postulated in studies by other authors. Estrogens stimulate proliferation of gonocytes [44,45], increase the number of spermatogonia A [46], and stimulate DNA synthesis in spermatogonia in the rat [47]. In human testis tissue cultures, estradiol has been shown to act as a germ cell survival factor [40].…”

Section: Discussionmentioning

confidence: 99%

Estrogen receptor alpha localization in the testes of men with normal spermatogenesis

Filipiak¹,

Suliborska²,

Walczak-Jędrzejowska³

et al. 2012

Folia Histochem Cytobiol.

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Abstract:It is known that estrogens act on the male reproductive tract by binding to estrogen receptors (ER) a and b. However, studies on ER localization in the human testis are discordant. The aim of this study was to investigate the localization of ERa in the testes of adult men with normal spermatogenesis. Semen analysis of ten adult men revealed azoospermia. FSH, LH and testosterone serum concentrations were within normal values, and the volume of the testes was normal, hence obstructive azoospermia was suspected. The tissues from testicular surgical biopsies were fixed in Bouin's fluid and embedded in paraffin. Assessments of the seminiferous epithelium (scoring 10 to -1), the number of Leydig cells (scoring 1 to 5), the areal fraction of intertubular space (IS), measurements of seminiferous tubule diameter, and the thickness of the tubular wall, were performed on microscopic sections. Immunohistochemical staining was applied with monoclonal antibodies against ERa. The mean spermatogenesis score was 10 points; IS -30.6 ± 8.1%; seminiferous tubule diameter -193.9 ± 19.4 μm; thickness of tubular wall -7.44 ± 1.1 μm; number of Leydig cells -1.6 ± 1.1 points. Immunohistochemical staining showed the localization of ERa to be in the Sertoli and Leydig cell cytoplasm, while ERa was absent in germ cells. The results of testicular tissue analysis confirmed its normal structure and normal, full spermatogenesis. The presence of ERa in Sertoli and Leydig cells in normal human testis demonstrated in this study suggests that estrogens may affect testicular function.

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“…Furthermore, gonocytes express RAF1 (v-rafleukemia viral oncogene 1), MAP2K1 (mitogen-activated protein kinase kinase 1), and MAPK1/3 (mitogen-activated protein kinase 1/3). Thuillier and colleagues reported that inhibiting RAF1 and MAP2K1 blocked both PDGF-and E2-induced gonocyte proliferation, placing these factors downstream in the pathways (Thuillier et al, 2010). Interestingly, E2 did not promote cycling in gonocytes in the absence of PDGF, highlighting its dependence.…”

Section: Ink4bmentioning

confidence: 99%

Cycling to and from a stem cell niche: the temporal and spatial odyssey of mitotic male germ cells

Payne

2013

Int. J. Dev. Biol.

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The development of male germ cells within the prenatal and prepubertal periods in mammals combines multiple biological events that integrate cell cycle regulation, epigenetic reprogramming, and cell migration along temporally and spatially dynamic lines. Germ cells arise from their precursor primordial germ cells in the mid-gestation embryo, forming gonocytes that enter G 0 phase cell cycle arrest within the fetal testis. Cyclin-dependent kinase inhibitors, activated retinoblastoma 1 protein, and increased levels of transforming growth factor beta 2 collectively influence this cell cycle arrest. Gonocyte quiescence persists until shortly after birth, whereupon the cells concomitantly re-enter the cell cycle and migrate towards a niche that establishes and maintains self-renewing spermatogonial stem cells and balances them with differentiating spermatogonia. Platelet-derived growth factor signaling is one of the mechanisms that regulates both mitotic activation and migration in neonatal gonocytes, along with mitogens, 17b-estradiol and retinoic acid, and chemoattractants C-C-motif ligand 9 and members of the ADAM, integrin, and tetraspanin families. Numerous germ cell-intrinsic proteins have been identified that ensure the retention of germ cells within the spermatogonial stem cell niche. Sertoli cells are a significant component of this niche, contributing essential growth factors and chemokines to spermatogonia. This review focuses on the dynamic events that occur to mitotic male germ cells before and during their arrival at this niche, with an emphasis on the cell cycle and directed migration.

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Interdependence of Platelet-Derived Growth Factor and Estrogen-Signaling Pathways in Inducing Neonatal Rat Testicular Gonocytes Proliferation1

Cited by 54 publications

References 67 publications

Mammalian gonocyte and spermatogonia differentiation: recent advances and remaining challenges

Mammalian gonocyte and spermatogonia differentiation: recent advances and remaining challenges

Estrogen receptor alpha localization in the testes of men with normal spermatogenesis

Cycling to and from a stem cell niche: the temporal and spatial odyssey of mitotic male germ cells

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