Fate determination of fetal Leydig cells

Wen, Quan; Liu, Yi‐Xun; Gao, Fei

doi:10.1007/s11515-011-1100-3

Cited by 7 publications

(7 citation statements)

References 56 publications

(50 reference statements)

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“…Moreover, using RNA-sequencing bioinformatics approach for analysis, a number of genes involved in neurogenesis/neurotransmission have been shown to be enriched in FLCs [28], supporting the notion that FLCs and neural cells could be originated from the same progenitor cell type. Thus, FLCs are derived from multiple and distinctive progenitor cells from adreno-gonadal primordium, coelomic epithelium, mesonephros, neural crest and early microvessels (for reviews, see [6,7]).…”

Section: Flc Cytogenesismentioning

confidence: 99%

“…FLC differentiation is known to be regulated strictly by Sertoli cells during fetal testis development (for a review, see [7]) (Fig. 2).…”

Section: Flc Cytogenesismentioning

confidence: 99%

“…While androstenedione-producing FLC population is gradually substituted by testosterone-producing ALCs during postnatal development, the mechanism(s) that governs this process remains unclear, and the fate of FLCs has been controversial [3,7]. Based on histological, morphological, ultrastructural and quantitative analysis of testes in rodents and humans during embryonic and postnatal development, FLCs are known to undergo gradual atrophy after birth, and the population of FLCs gradually vanishes via degeneration in adult testes without involving apoptosis [9,43–45] (Fig.…”

Section: Flc Cytogenesismentioning

confidence: 99%

“…Subsequent studies have identified two distinct Leydig cell populations namely FLCs and adult Leydig cells (ALCs) which are found in fetal and adult testes, respectively, during testis development in most species (for a review, see [6]). FLCs differentiate in the fetal testes by embryonic day 12.5 (E12.5) to E13.5 in rodents; after birth, FLCs undergo gradual atrophy, also known as involution or degeneration, and being replaced by ALCs in postnatal 2–3 weeks [7,8]. However, FLC atrophy is not an apoptotic process [9], and ALCs do not originate from FLCs [10,11], thus, the fate of FLCs remains controversial for years based on morphological analysis (for a review, see [7]).…”

Section: Introductionmentioning

confidence: 99%

“…FLCs differentiate in the fetal testes by embryonic day 12.5 (E12.5) to E13.5 in rodents; after birth, FLCs undergo gradual atrophy, also known as involution or degeneration, and being replaced by ALCs in postnatal 2–3 weeks [7,8]. However, FLC atrophy is not an apoptotic process [9], and ALCs do not originate from FLCs [10,11], thus, the fate of FLCs remains controversial for years based on morphological analysis (for a review, see [7]). Recent studies using FLC specific lineage tracing methods have shown that FLCs persist in adult mouse testes as a subpopulation together with ALCs, constituted about ~20% of the total Leydig cell population [10,11].…”

Section: Introductionmentioning

confidence: 99%

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Development, function and fate of fetal Leydig cells

Wen

Cheng

Liu

2016

Seminars in Cell & Developmental Biology

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107

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During fetal testis development, fetal Leydig cells (FLCs) are found to be originated from multiple progenitor cells. FLC specification and function are under tight regulation of specific genes and signaling proteins. Furthermore, Sertoli cells play a crucial role to regulate FLC differentiation during fetal testis development. FLC progenitor- and FLC-produced biomolecules are also involved in the differentiation and activity of rodent FLCs. The main function of FLCs is to produce androgens to masculinize XY embryos. However, FLCs are capable of producing androstenedione but not testosterone due to the lack of 17β-HSD (17β-hydroxysteroid dehydrogenase), but fetal Sertoli cells express 17β-HSD which thus transforms androstenedione to testosterone in the fetal testis. On the other hand, FLCs produce activin A to regulate Sertoli cell proliferation, and Sertoli cells in turn modulate testis cord expansion. It is now generally accepted that adult Leydig cells (ALCs) gradually replace FLCs during postnatal development to produce testosterone to support spermatogenesis as FLCs undergo degeneration in neonatal and pre-pubertal testes. However, based on studies using genetic tracing mouse models, FLCs are found to persist in adult testes, making up ~20% of total Leydig cells. In this review, we evaluate the latest findings regarding the development, function and fate of FLCs during fetal and adult testis development.

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Section: Flc Cytogenesismentioning

confidence: 99%

“…FLC differentiation is known to be regulated strictly by Sertoli cells during fetal testis development (for a review, see [7]) (Fig. 2).…”

Section: Flc Cytogenesismentioning

confidence: 99%

Section: Flc Cytogenesismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Development, function and fate of fetal Leydig cells

Wen

Cheng

Liu

2016

Seminars in Cell & Developmental Biology

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107

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Calretinin Immunoreactivity in the Human Testis Throughout Fetal Life

Altobelli

Pentimalli

D’Armiento

et al. 2017

Journal Cellular Physiology

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The main functions of the testis are sex hormone and sperm cell production. Steroidogenesis occurs in the Leydig interstitial cells and spermatogenesis in the seminiferous tubules. Male gonad morphogenesis is a finely orchestrated process, mainly coordinated by hormones, whose actions can significantly affect post-pubertal testicular function. Calcium is a key intracellular messenger, which regulates many signal transduction pathways, and is also implicated in steroidogenesis. Calcium homeostasis and signaling rely on many calcium-binding proteins including calretinin, of the "EF-hand" protein family. Calretinin is a highly conserved protein mainly expressed in the nervous system but also detected in rat and human adult and fetal testis as well as in pathological conditions. Calretinin expression in the fetal testis, however, has not been thoroughly analyzed probably owing to limited availability and paucity of tissues. Here, we examined by immunocytochemistry the expression of calretinin in human fetal testis specimens, obtained from natural and therapeutic abortions, at various developmental ages. We found that calretinin-immunoreactive Leydig cells were visible throughout the timeframe studied (14th-27th week). Immunoreactivity was also observed in Sertoli cells and in the germ cells of the immature seminiferous tubules. Overall our data indicate that calretinin expression parallels the decline in Leydig cell number, suggesting that its presence is indeed correlated to their steroidogenic activity. They also suggest that the intratubular positivity of calretinin could be linked to the ability of Sertoli cells to produce locally acting hormones contributing to the histodifferentiation of the male genital tract. J. Cell. Physiol. 232: 1872-1878, 2017. © 2016 Wiley Periodicals, Inc.

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