The postnatal development of the junctional complexes of the mouse Sertoli cells as revealed by freeze‐fracture

Nagano, Toshio; Suzuki, Fumie

doi:10.1002/ar.1091850403

Cited by 139 publications

(78 citation statements)

References 28 publications

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“…This example of a claudin shows a transient association with TJs at the time of their formation. TJs form during puberty coincident with a rise in testosterone and expression of the androgen receptor in Sertoli cells (35). To determine whether Cldn3 is expressed during initial TJ formation in pubertal animals, we killed mice at various ages and examined Cldn3 expression.…”

Section: Resultsmentioning

confidence: 99%

Androgens regulate the permeability of the blood–testis barrier

Meng

Holdcraft

Shima

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

362

348

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Within the mammalian testis, specialized tight junctions between somatic Sertoli cells create basal and apical polarity within the cells, restrict movement of molecules between cells, and separate the seminiferous epithelium into basal and adluminal compartments. These tight junctions form the basis of the blood-testis barrier, a structure whose function and dynamic regulation is poorly understood. In this study, we used microarray gene expression profiling to identify genes with altered transcript levels in a mouse model for conditional androgen insensitivity. We show that testosterone, acting through its receptor expressed in Sertoli cells, regulates the expression of claudin 3, which encodes a transient component of newly formed tight junctions. Sertoli cell-specific ablation of androgen receptor results in increased permeability of the bloodtestis barrier to biotin, suggesting claudin 3 regulates the movement of small molecules across the Sertoli cell tight junctions. These results suggest that androgen action in Sertoli cells regulates germ cell differentiation, in part by controlling the microenvironment of the seminiferous epithelium. Our studies also indicate that hormonal strategies for male contraception may interfere with the blood-testis barrier.androgen receptor ͉ testosterone ͉ tight junctions

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Section: Resultsmentioning

confidence: 99%

Androgens regulate the permeability of the blood–testis barrier

Meng

Holdcraft

Shima

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

362

348

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“…Gap junctions between neonatal Sertoli cells have also been documented (Nagano and Suzuki, 1976). Change of Cx43 spatial distribution in Sertoli cells from their apical region (3 dpp) to their basal domain (14 dpp) is correlated with the differentiation from a nonpolarized to a polarized epithelium (Vergoween et al, 1991).…”

Section: Bmentioning

confidence: 97%

“…Change of Cx43 spatial distribution in Sertoli cells from their apical region (3 dpp) to their basal domain (14 dpp) is correlated with the differentiation from a nonpolarized to a polarized epithelium (Vergoween et al, 1991). By the end of the second week post partum, the lumen of the tubule is formed (Flickinger, 1967) and gap junctions (Gilula et al, 1976;Nagano and Suzuki, 1976) and tight-junction protein ZO-1 (Byers et al, 1991) distribution changes from the apical to the basal pole of Sertoli cells. More recently, direct interaction (Giepmans and Moolenaar, 1998) and co-localization of the tight junction protein ZO-1 with Cx43 has been documented (Batias et al, 1999).…”

Section: Bmentioning

confidence: 99%

Expression of Connexin43 in mouse Leydig, Sertoli, and germinal cells at different stages of postnatal development

et al. 2001

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Connexin 43 (Cx43) is the most abundant and ubiquitously distributed gap junction protein in testicular cells. Lack of Cx43 expression results in male infertility. We investigated whether Cx43 is expressed and regulated in Leydig, Sertoli and germinal cells at different stages of postnatal development. Cx43 was detected using three different antibodies shown by immunoblotting to be highly specific. At different postnatal ages Cx43 localization was compared in serial or double labeled testicular cryosections with immunocytochemical distribution of steroidogenic enzyme, 3 ␤hidroxysteroid-dehydrogenase (3␤HSD), Mullerian inhibitory hormone (MIH), and germinal nuclear cell antigen (GNCA1), which are specific markers of interstitial Leydig, Sertoli and germinal cells, respectively. In the interstitium, round cell clumps (RCC) with lipid droplets positive for 3␤HSD and Cx43 were frequently found at intertubular areas at birth and Cx43 was mainly localized at cell membrane appositions. From day 3, the number and size of 3␤HSD-positive RCC started to decrease, and reached a minimum at 7-14 dpp; Cx43 expressed by them is progressively downregulated. From day 21 an increase in the size and number of RCC positive for Cx43 and 3␤HSD was found that continued at 24, 26 and 28 days and reached a maximum at 35 and 60 dpp. Biphasic expression of interstitial Cx43 and 3␤HSD was also found to be positively and temporally correlated with fluctuations in intratesticular testosterone content at all ages studied. In the seminiferous cord (SC), Cx43 was expressed at birth between adjacent Sertoli cells (MIH positive) localized at the periphery, as well as in their cytoplasm projections that surround centrally localized gonocytes. From days 3 to 7, Cx43 labeling increased in Sertoli cells mainly at their apical border. At day 14, Cx43 distribution in Sertoli cells changed from apical to basal in parallel to migration of germinal (GNCA1-positive) cells from the periphery to the center of the SC. At all these ages, Cx43 was also localized at cell borders between Sertoli and germinal cells. In conclusion, this study demonstrates that Cx43 in Leydig cells is regulated during postnatal development in an age and functional dependent manner. In the tubule, it is demonstrated that Cx43 is modulated in Sertoli cells during the neonatal and prepubertal period. We also provide evidence for the first time that Cx43-gap junctions communicate between Sertoli and germinal cells before and during the first wave of spermatogenesis. Anat Rec 264: [13][14][15][16][17][18][19][20][21][22][23][24] 2001.

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“…In the seminiferous tubules, this is particularly evident between SC and their BTB (Mruk & Cheng 2004, Brehm & Steger 2005, Bergmann 2006, Li et al 2012. Ocln codes for the tight junction protein OCCLUDIN (Furuse et al 1998) and is believed to be the initiator for BTB formation (Nagano & Suzuki 1976), although it is yet detectable in fetal murine SC (Cyr et al 1999). BTB formation due to OCCLUDIN expression begins at around day 10 postpartum and correlates with the initiation of spermatogenesis (Cyr et al 1999, Gerber et al 2014.…”

Section: Sc Btb and Junctional Proteinsmentioning

confidence: 99%

“…It is believed that OCCLUDIN initially forms the BTB at the beginning of spermatogenesis (Nagano & Suzuki 1976) and it was significantly upregulated in the adult KO mice . Gerber et al (2014) demonstrated that pubertal KO mice exhibit a 1 day delay in OCCLUDIN localisation towards the BTB region when compared with their WT littermates (Fig.…”

Section: Sccx43ko Mice and Btbmentioning

confidence: 99%

Blood–testis barrier and Sertoli cell function: lessons from SCCx43KO mice

Gerber¹,

Heinrich²,

Brehm³

2016

Reproduction

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The gap junction protein connexin43 (CX43) plays a vital role in mammalian spermatogenesis by allowing for direct cytoplasmic communication between neighbouring testicular cells. In addition, different publications suggest that CX43 in Sertoli cells (SC) might be important for blood-testis barrier (BTB) formation and BTB homeostasis. Thus, through the use of the Cre-LoxP recombination system, a transgenic mouse line was developed in which only SC are deficient of the gap junction protein, alpha 1 (Gja1) gene. Gja1 codes for the protein CX43. This transgenic mouse line has been commonly defined as the SC specific CX43 knockout (SCCx43KO) mouse line. Within the seminiferous tubule, SC aid in spermatogenesis by nurturing germ cells and help them to proliferate and mature. Owing to the absence of CX43 within the SC, homozygous KO mice are infertile, have reduced testis size, and mainly exhibit spermatogenesis arrest at the level of spermatogonia, seminiferous tubules containing only SC (SC-only syndrome) and intratubular SC-clusters. Although the SC specific KO of CX43 does not seem to have an adverse effect on BTB integrity, CX43 influences BTB composition as the expression pattern of different BTB proteins (like OCCLUDIN, b-CATENIN, N-CADHERIN, and CLAUDIN11) is altered in mutant males. The supposed roles of CX43 in dynamic BTB regulation, BTB assembly and/or disassembly and its possible interaction with other junctional proteins composing this unique barrier are discussed. Data collectively indicate that CX43 might represent an important regulator of dynamic BTB formation, composition and function.Reproduction (2016) 151 R15-R27

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The postnatal development of the junctional complexes of the mouse Sertoli cells as revealed by freeze‐fracture

Cited by 139 publications

References 28 publications

Androgens regulate the permeability of the blood–testis barrier

Androgens regulate the permeability of the blood–testis barrier

Expression of Connexin43 in mouse Leydig, Sertoli, and germinal cells at different stages of postnatal development

Blood–testis barrier and Sertoli cell function: lessons from SCCx43KO mice

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