Testosterone upregulation of tissue type plasminogen activator expression in Sertoli cells

Guo, Jian; Shi, Yu; Yang, Wei; Li, Yin Chuan; Zhao, Hu; Liu, Yi Xun

doi:10.1007/s12020-007-9014-1

Cited by 15 publications

(15 citation statements)

References 50 publications

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“…In these altered genes, the genes from signaling pathways for cell adhesion, focal adhesions, tight junctions and gap junctions were enriched ( Supplemental Fig. 4 ), including junction genes (Cx43, JAMA, claudin11, claudin1, claudin5) and BTB regulators (matrix metalloproteinase 2 (MMP2), MMP17, intercellular adhesion molecule 1 (ICAM1) and tissue-type plasminogen activator (TPA)) 40 41 42 ( Fig. 3C , left table).…”

Section: Resultsmentioning

confidence: 99%

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Deletion of the tyrosine phosphatase Shp2 in Sertoli cells causes infertility in mice

Tang

et al. 2015

Sci Rep

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The male’s ability to reproduce is completely dependent on Sertoli cells. However, the mechanisms governing the functional integrity of Sertoli cells have remained largely unexplored. Here, we demonstrate that deletion of Shp2 in Sertoli cells results in infertility in mice. In Shp2 knockout mice (SCSKO), a normal population of Sertoli cells was observed, but the blood-testis barrier (BTB) was not formed. Shp2 ablation initiated the untimely and excessive differentiation of spermatogonial stem cells (SSCs) by disturbing the expression of paracrine factors. As a consequence, the process of spermatogenesis was disrupted, and the germ cells were depleted. Furthermore, Shp2 deletion impaired the cell junctions of the primary Sertoli cells and failed to support the clonal formation of SSCs co-cultured with SCSKO Sertoli cells. As expected, Shp2 restoration largely restores the cell junctions of the primary Sertoli cells and the clonal formation of SSCs. To identify the underlying mechanism, we further demonstrated that the absence of Shp2 suppressed Erk phosphorylation, and thus, the expression of follicle-stimulating hormone (FSH)- and testosterone-induced target genes. These results collectively suggest that Shp2 is a critical signaling protein that is required to maintain Sertoli cell function and could serve as a novel target for male infertility therapies.

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Section: Resultsmentioning

confidence: 99%

“…3B and unpublished data). Furthermore, Shp2 deletion altered the expression of several junction genes, such as claudin 1, claudin 11 and TPA 40 42 . These results suggested that Shp2 mediates BTB formation by regulating the expression and localization of junctional complex proteins.…”

Section: Disscussionmentioning

confidence: 99%

Deletion of the tyrosine phosphatase Shp2 in Sertoli cells causes infertility in mice

Tang

et al. 2015

Sci Rep

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“…In adulthood, FSH drives Sertoli cells to produce regulatory molecules and nutrients required for spermatogenesis [18]. In particular, FSH activates the transcription of genes involved in metabolic homeostasis and supports germ cell functions [16], with the synthesis of retinoic acid, lactate, type 2 plasminogen activator, as well as fatty acid metabolism and mitochondrial biogenesis [19,20]. FSH circulating levels correlate directly with Sertoli cell number and testicular volume in adults [21].…”

Section: Physiological Control Of Spermatogenesismentioning

confidence: 99%

Follicle-Stimulating Hormone (FSH) Action on Spermatogenesis: A Focus on Physiological and Therapeutic Roles

Santi

Crépieux

Reiter

et al. 2020

JCM

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Background: Human reproduction is regulated by the combined action of the follicle-stimulating hormone (FSH) and the luteinizing hormone (LH) on the gonads. Although FSH is largely used in female reproduction, in particular in women attending assisted reproductive techniques to stimulate multi-follicular growth, its efficacy in men with idiopathic infertility is not clearly demonstrated. Indeed, whether FSH administration improves fertility in patients with hypogonadotropic hypogonadism, the therapeutic benefit in men presenting alterations in sperm production despite normal FSH serum levels is still unclear. In the present review, we evaluate the potential pharmacological benefits of FSH administration in clinical practice. Methods: This is a narrative review, describing the FSH physiological role in spermatogenesis and its potential therapeutic action in men. Results: The FSH role on male fertility is reviewed starting from the physiological control of spermatogenesis, throughout its mechanism of action in Sertoli cells, the genetic regulation of its action on spermatogenesis, until the therapeutic options available to improve sperm production. Conclusion: FSH administration in infertile men has potential benefits, although its action should be considered by evaluating its synergic action with testosterone, and well-controlled, powerful trials are required. Prospective studies and new compounds could be developed in the near future.

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“…3). Sertoli and granulosa cells express enzymes that cleave proAMH, with the levels of the enzymes and/or their regulators varying during testicular (Nachtigal & Ingraham 1996, Guo et al 2007, Le Magueresse-Battistoni 2007, Uhrin et al 2007) and ovarian (Bae et al 2008) development, the seminiferous cycle (Guo et al 2007, Le Magueresse-Battistoni 2007, Uhrin et al 2007, the ovarian cycle (Bae et al 2008, Wang et al 2014, the stage of ovarian follicular development (Ohnishi et al 2005, Bae et al 2008, Antenos et al 2011) and during pregnancy (Kwok et al 2013). However, the AMH in ovine follicular fluid is predominantly proAMH with little AMH N,C (Campbell et al 2012), suggesting that AMH can be synthesised and released with little or no prior cleavage.…”

Section: Gonadal Cleavage Of Proamhmentioning

confidence: 99%

Anti-Müllerian hormone is a gonadal cytokine with two circulating forms and cryptic actions

McLennan¹,

Pankhurst²

2015

Journal of Endocrinology

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Anti-Mü llerian hormone (AMH) is a multi-faceted gonadal cytokine. It is present in all vertebrates with its original function in phylogeny being as a regulator of germ cells in both sexes, and as a prime inducer of the male phenotype. Its ancient functions appear to be broadly conserved in mammals, but with this being obscured by its overt role in triggering the regression of the Mü llerian ducts in male embryos. Sertoli and ovarian follicular cells primarily release AMH as a prohormone (proAMH), which forms a stable complex (AMH N,C ) after cleavage by subtilisin/kexin-type proprotein convertases or serine proteinases. Circulating AMH is a mixture of proAMH and AMH N,C , suggesting that proAMH is activated within the gonads and putatively by its endocrine target-cells. The gonadal expression of the cleavage enzymes is subject to complex regulation, and the preliminary data suggest that this influences the relative proportions of proAMH and AMH N,C in the circulation. AMH shares an intracellular pathway with the bone morphogenetic protein (BMP) and growth differentiation factor (GDF) ligands. AMH is male specific during the initial stage of development, and theoretically should produce male biases throughout the body by adding a male-specific amplification of BMP/GDF signalling. Consistent with this, some of the male biases in neuron number and the non-sexual behaviours of mice are dependent on AMH. After puberty, circulating levels of AMH are similar in men and women. Putatively, the function of AMH in adulthood maybe to add a gonadal influence to BMP/GDF-regulated homeostasis.

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Testosterone upregulation of tissue type plasminogen activator expression in Sertoli cells

Cited by 15 publications

References 50 publications

Deletion of the tyrosine phosphatase Shp2 in Sertoli cells causes infertility in mice

Deletion of the tyrosine phosphatase Shp2 in Sertoli cells causes infertility in mice

Follicle-Stimulating Hormone (FSH) Action on Spermatogenesis: A Focus on Physiological and Therapeutic Roles

Anti-Müllerian hormone is a gonadal cytokine with two circulating forms and cryptic actions

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