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Frontiers in Biology

ISSN 1674-7984

ISSN 1674-7992(Online)

CN 11-5892/Q

Front Biol    2011, Vol. 06 Issue (01) : 12-18    https://doi.org/10.1007/s11515-011-1100-3
REVIEW
Fate determination of fetal Leydig cells
Qing WEN1,2, Yixun LIU1(), Fei GAO1()
1. State Key Laboratory of Reproduction Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China; 2. Graduate School of the Chinese Academy of Sciences, Beijing 100049, China
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Abstract

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.

Keywords fetal Leydig cells      adult Leydig cells      fate determination     
Corresponding Author(s): LIU Yixun,Email:liuyixun@ioz.ac.cn; GAO Fei,Email:gaofei72@yahoo.com   
Issue Date: 01 February 2011
 Cite this article:   
Qing WEN,Yixun LIU,Fei GAO. Fate determination of fetal Leydig cells[J]. Front Biol, 2011, 06(01): 12-18.
 URL:  
https://academic.hep.com.cn/fib/EN/10.1007/s11515-011-1100-3
https://academic.hep.com.cn/fib/EN/Y2011/V06/I01/12
Fig.1  Leydig cell differentiation exhibits a biphasic pattern in mouse testes. Original magnification, × 400. Immunohistochemistry staining for Leydig cell marker, 3-beta–hydroxysteroid dehydrogenase (3β-HSD) A, E15.5 testis, FLCs are present in the testicular interstitium (arrow). B, postnatal day 1(D1) testis, more FLCs are noted in the testis (arrow). C, D7 testis, very few normal FLCs are found between the seminiferous tubules, most of them may undergo involution or degeneration postnatally (arrow). D, D21 testis, immature ALCs appear (arrow). ST, seminiferous tubule.
Fig.1  Leydig cell differentiation exhibits a biphasic pattern in mouse testes. Original magnification, × 400. Immunohistochemistry staining for Leydig cell marker, 3-beta–hydroxysteroid dehydrogenase (3β-HSD) A, E15.5 testis, FLCs are present in the testicular interstitium (arrow). B, postnatal day 1(D1) testis, more FLCs are noted in the testis (arrow). C, D7 testis, very few normal FLCs are found between the seminiferous tubules, most of them may undergo involution or degeneration postnatally (arrow). D, D21 testis, immature ALCs appear (arrow). ST, seminiferous tubule.
Fig.2  FLCs and ALCs in mouse testis. Original magnification, × 400. Oil Red O staining is performed on frozen section of D1 (A) and D56 (B) mouse testes. A, FLCs with characteristic large lipid droplets (red) are arranged exclusively in cluster (arrows). B, ALCs with small lipid droplets (red). ST, seminiferous tubule.
Fig.2  FLCs and ALCs in mouse testis. Original magnification, × 400. Oil Red O staining is performed on frozen section of D1 (A) and D56 (B) mouse testes. A, FLCs with characteristic large lipid droplets (red) are arranged exclusively in cluster (arrows). B, ALCs with small lipid droplets (red). ST, seminiferous tubule.
Fig.3  Ultrastructure of a mouse FLC and ALC. A, Original magnification, × 4000. FLC contains mitochondria with tubulo-vesicular cristae (white arrowheads), SER (black arrow), and large round clustered lipid droplets (diameter= 0.9 μm, white arrow). B, Original magnification, × 6000. A large amount of SER (black arrow), numerous mitochondria with tubulo-vesicular cristae(white arrowheads), and a few dispersed small lipid droplets (diameter= 0.5 μm, white arrow) are present in ALC.
Fig.3  Ultrastructure of a mouse FLC and ALC. A, Original magnification, × 4000. FLC contains mitochondria with tubulo-vesicular cristae (white arrowheads), SER (black arrow), and large round clustered lipid droplets (diameter= 0.9 μm, white arrow). B, Original magnification, × 6000. A large amount of SER (black arrow), numerous mitochondria with tubulo-vesicular cristae(white arrowheads), and a few dispersed small lipid droplets (diameter= 0.5 μm, white arrow) are present in ALC.
FeaturesIn fetal LCIn adult LCCommon in both types
NucleusRound with smooth membranesElliptic or round with curly membranesThick euchromatin, numerous nuclear pores
SERPresent in abundance
Rough ERLargely absentOnly a few
MitochondriaTubulo-vesicular cristae
Golgi apparatusSmall to moderate sizeLarge and well differentiated
Lipid dropletsNumerous (diameter= 0.9 μm)A few (diameter= 0.5 μm)
Cell contactsWith other FLCsWith ALCs and fibroblasts25 nm space contacts with adjacent LC
MicrovilliAccumulation in localized spaces
SurfaceNumerous (finger-like protrusions)A few, small protrusions
Basal laminaPresent (of various thickness)Absent
ArrangedIn clustersNot exclusively in clusters
Tab.1  A comparison of ultrastructural features of fetal and ALCss
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