2012
DOI: 10.1016/j.mce.2012.02.018
|View full text |Cite
|
Sign up to set email alerts
|

Activins and inhibins in mammalian testis development: New models, new insights

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
23
0

Year Published

2013
2013
2021
2021

Publication Types

Select...
5
2

Relationship

0
7

Authors

Journals

citations
Cited by 43 publications
(23 citation statements)
references
References 128 publications
0
23
0
Order By: Relevance
“…Thus, the absence of STK35 does not appear to directly cause a deficiency in Sertoli cell maturation status that would drive germ cell loss from the seminiferous epithelium (Rajpert-De Meyts et al, 1999; Russell et al, 1990; Sharpe et al, 2003); instead, we hypothesize the deficiency is intrinsic to germ cells arising from the absence of a vital gene product(s) from the STK35 locus. Initiation of postnatal spermatogenesis involves germ cell migration to the seminiferous epithelium basement membrane (Barakat et al, 2012), while subsequent spermatogenic stages feature progressive movement towards the tubule lumen (Mruk and Cheng, 2004; Siu and Cheng, 2004), hence an inability to migrate could lead to germ cell loss. STK35L1 involvement in migration has been demonstrated in an endothelial cell line (Goyal et al, 2011), and we speculate this could be one important function of a STK35 gene product in spermatogenesis.…”
Section: Discussionmentioning
confidence: 99%
“…Thus, the absence of STK35 does not appear to directly cause a deficiency in Sertoli cell maturation status that would drive germ cell loss from the seminiferous epithelium (Rajpert-De Meyts et al, 1999; Russell et al, 1990; Sharpe et al, 2003); instead, we hypothesize the deficiency is intrinsic to germ cells arising from the absence of a vital gene product(s) from the STK35 locus. Initiation of postnatal spermatogenesis involves germ cell migration to the seminiferous epithelium basement membrane (Barakat et al, 2012), while subsequent spermatogenic stages feature progressive movement towards the tubule lumen (Mruk and Cheng, 2004; Siu and Cheng, 2004), hence an inability to migrate could lead to germ cell loss. STK35L1 involvement in migration has been demonstrated in an endothelial cell line (Goyal et al, 2011), and we speculate this could be one important function of a STK35 gene product in spermatogenesis.…”
Section: Discussionmentioning
confidence: 99%
“…Interestingly, in co-cultured immature mouse spermatogonia and Sertoli cells, BMP2 and BMP4 stimulate the expression of Smad1, Smad5 and Smad8 in spermatogonia nuclei [115,167]. As described before, the BMPs control the balanced growth of spermatogonial cells and their niches in a stage specific way during mammalian embryonic, post-natal and adult testis organogenesis [133,134].…”
Section: Bone Morphogenetic Factors: Germ Cell Maintenance Differentmentioning
confidence: 75%
“…Finally, it is important to stress that SSC niche function varies in a dynamic way during mammalian development (embryonic, post-natal and adult stages) [106,131]. This is supported by studying niche stimulation via the gonadotropin-realising hormone (GnRH) [132], TGFβ signaling components [133,134] and SSC transplantation assays showing that immature mouse pup testes can support the colonization and proliferation of transplanted SSCs much better than in adult testes [135]. These studies provide evidence that the male stem cell niche and spermatogenesis in mammals undergoes dramatic stage-specific changes during testis development and maturation.…”
Section: The Mammalian Testis Niche: a Flexible Unit For Stem Cell Mamentioning
confidence: 99%
See 1 more Smart Citation
“…Importantly, the initial ovarian follicular growth and development are mediated by complex interactions between the oocyte and peripheral immune factors, such as cytokines, chemokines and growth factors [86,87,88]. Similarly in males, growth factors and cytokines are crucial in the regulation of testicular spermatogenesis and steroidogenesis [89,90]. Therefore, the impact of perinatal immune challenge on the early development of reproductive organs may be mediated via peripheral factors to a greater extent than via central mechanisms.…”
Section: Impact Of Perinatal Lps Exposure On Reproductive Functionmentioning
confidence: 99%