Fetal and Adult Leydig Cells Are of Common Orig

Davidoff, M; Middendorff, Ralf; Müller, Dieter; Holstein, A. F.

doi:10.1007/978-3-642-00513-8_8

Cited by 4 publications

(3 citation statements)

References 162 publications

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“…Thus, FLCs originate from the testis interstitial compartment which contains MAFB (v-maf musculoaponeurotic fibrosarcoma oncogene family, protein B) positive cells migrated from the coelomic epithelia [15,16], and MAFB and/or VCAM1 (vascular cell adhesion molecule 1) positive cells from the gonad–mesonephros border [15,17–19]. Other studies also suggest that cells derived from neural crest [20–22], and pericytes (for a review, see [23]) that invade developing testes with coelomic vessel are also the source of FLC progenitors. However, there is no direct evidence supporting the pericyte origination hypothesis, and lineage tracing experiments using mouse models have shown no evidence of neural crest cell contribution to FLC population [24].…”

Section: Flc Cytogenesismentioning

confidence: 99%

Development, function and fate of fetal Leydig cells

Wen

Cheng

Liu

2016

Seminars in Cell & Developmental Biology

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%

Development, function and fate of fetal Leydig cells

Wen

Cheng

Liu

2016

Seminars in Cell & Developmental Biology

107

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“…However, lineage tracing experiments using knockout mice models found no evidence of neural crest contribution to FLCs population (Brennan et al, 2003). Testicular vasculature appears between E11.5 and E12.5 (Brennan and Capel, 2004), which is closely associated with the emergence of FLCs (Davidoff et al, 2009). Therefore, it is presumed that the pericyte, a source of stem cells of vascular wall, could also contribute to the FLCs (Brennan and Capel, 2004).…”

Section: Origin Of Flcsmentioning

confidence: 95%

“…These evidences suggest that FLCs could derive from multiple sources (Yao and Barsoum, 2007;Davidoff et al, 2009). …”

Section: Origin Of Flcsmentioning

confidence: 96%

Fate determination of fetal Leydig cells

2011

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Leydig cell (LC) is one of the most important somatic cell types in testis, which localized in the interstitium between seminiferous tubules. The major function of Leydig cells is to produce steroid hormone, androgens. LC differentiation exhibits a biphasic pattern in rodent testes, which are divided into two different temporal mature populations, fetal Leydig cells (FLCs) and adult Leydig cells (ALCs). FLCs are transiently present in fetal testes and undergo involution or degeneration after birth. FLCs are completely devoid and replaced by ALCs in adult testes. Comparing to ALCs, FLCs display unique morphology, ultrastructure and functions. The origin of FLCs has been debated for many years, but it is still a mystery. Many factors have been reported regulating the specification, proliferation and differentiation of FLCs. FLCs degenerate in a few weeks postnatally, however, the underlying mechanism is still unknown. In this review, we will focus on the fate determination of FLCs, and summarize the resent progress on the morphology, ultrastructure, function, origin and involution of FLCs.

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Functional Anatomy and Histology of the Testis

Fietz

Bergmann

2017

Endocrinology

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Fetal and Adult Leydig Cells Are of Common Orig

Cited by 4 publications

References 162 publications

Development, function and fate of fetal Leydig cells

Development, function and fate of fetal Leydig cells

Fate determination of fetal Leydig cells

Functional Anatomy and Histology of the Testis

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