Understanding spermatogenesis is a prerequisite for treatment

Holstein, A. F.; Schulze, Wolfgang; Davidoff, M

doi:10.1186/1477-7827-1-107

Cited by 188 publications

(68 citation statements)

References 29 publications

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“…It involves four key cellular events, namely (i) spermatogoniogenesis (a continuous process that involves division of type A spermatogonia, which maintains a pool of stem cells, and the production of type B spermatogonia whose fate is to develop into spermatozoa), (ii) spermatocyte differentiation, (iii) spermiogenesis (a process in which spermatids undergo morphogenesis to become mature and motile spermatozoa) and (iv) spermiation (the release of elongated spermatids or spermatozoa, the end-product of spermatogenesis) into the lumen of the seminiferous epithelium (Holstein et al 2003). Besides developing germ cells, the seminiferous epithelium is also composed of a somatic constituent: the Sertoli cell, a 'nurse-like' cell known to provide nutritional and structural support to developing germ cells (Bardin et al 1988;Griswold & McLean 2006).…”

Section: Introductionmentioning

confidence: 99%

Sertoli–germ cell junctions in the testis: a review of recent data

Kopera

Bilińska

Cheng

et al. 2010

Phil. Trans. R. Soc. B

143

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Spermatogenesis is a process that involves an array of cellular and biochemical events, collectively culminating in the formation of haploid spermatids from diploid precursor cells known as spermatogonia. As germ cells differentiate from spermatogonia into elongated spermatids, they also progressively migrate across the entire length of the seminiferous epithelium until they reach the luminal edge in anticipation of spermiation at late stage VIII of spermatogenesis. At the same time, these germ cells must maintain stable attachment with Sertoli cells via testis-unique intermediate filament-(i.e. desmosome-like junctions) and actin-(i.e. ectoplasmic specializations, ESs) based cell junctions to prevent sloughing of immature germ cells from the seminiferous epithelium, which may result in infertility. In essence, both desmosome-like junctions and basal ESs are known to coexist between Sertoli cells at the level of the blood -testis barrier where they cofunction with the well-studied tight junction in maintaining the immunological barrier. However, the type of anchoring device that is present between Sertoli and germ cells depends on the developmental stage of the germ cell, i.e. desmosome-like junctions are present between Sertoli and germ cells up to, but not including, step 8 spermatids after which this junction type is replaced by the apical ES. While little is known about the biology of the desmosome-like junction in the testis, we have a relatively good understanding of the molecular architecture and the regulation of the ES. Here, we discuss recent findings relating to these two junction types in the testis, highlighting prospective areas that should be investigated in future studies.

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Section: Introductionmentioning

confidence: 99%

Sertoli–germ cell junctions in the testis: a review of recent data

Kopera

Bilińska

Cheng

et al. 2010

Phil. Trans. R. Soc. B

143

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“…Sertoli cells are large, somatic cells, contacting the basal lamina of the seminiferous tubules and extending to the lumen of tubules (Holstein et al, 2003). Germ cells comprise a stem cell population of basal spermatogonia and a migrating population undergoing the morphological and functional differentiation called spermatogenesis.…”

Section: Discussionmentioning

confidence: 99%

Polydeoxyribonucleotide, an Adenosine-A2A Receptor Agonist, Preserves Blood Testis Barrier from Cadmium-Induced Injury

et al. 2017

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Cadmium (Cd) impairs blood-testis barrier (BTB). Polydeoxyribonucleotide (PDRN), an adenosine A2A agonist, has positive effects on male reproductive system. We investigated the effects of PDRN on the morphological and functional changes induced by Cd in mice testes. Adult Swiss mice were divided into four groups: controls administered with 0.9% NaCl (1 ml/kg, i.p., daily) or with PDRN (8 mg/kg, i.p. daily), animals challenged with Cd chloride (CdCl2; 2 mg/kg, i.p, daily) and animals challenged with CdCl2 (2 mg/kg, i.p., daily) and treated with PDRN (8 mg/kg, i.p., daily). Experiments lasted 14 days. Testes were processed for biochemical, structural, and ultrastructural evaluation and hormones were assayed in serum. CdCl2 increased pERK 1/2 expression and Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH) levels; it decreased testosterone (TE) and inhibin-B levels and induced structural damages in extratubular compartment and in seminiferous epithelium, with ultrastructural features of BTB disruption. Many TUNEL-positive germ cells were present. CdCl2 increased tubular TGF-β3 immunoreactivity and reduced claudin-11, occludin, and N-cadherin immunoreactivity. PDRN administration reduced pERK 1/2 expression, FSH, and LH levels; it increased TE and inhibin-B levels, ameliorated germinal epithelium changes and protected BTB ultrastructure. Few TUNEL-positive germ cells were present and the extratubular compartment was preserved. Furthermore, PDRN decreased TGF-β3 immunoreactivity and enhanced claudin-11, occludin, and N-cadherin immunoreactivity. We demonstrate a protective effect of PDRN on Cd-induced damages of BTB and suggest that PDRN may play an important role against Cd, particularly against its harmful effects on gametogenesis.

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“…SCs play an essential role in developing sperm cells at all stages of spermatogenesis42. They provide physical support, nutrients, and paracrine signals to all germ cell generations43.…”

Section: Discussionmentioning

confidence: 99%

OSR1 and SPAK cooperatively modulate Sertoli cell support of mouse spermatogenesis

Liu

Yang

Chen

et al. 2016

Sci Rep

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We investigated the role of oxidative stress-responsive kinase-1 (OSR1) and STE20 (sterile 20)/SPS1-related proline/alanine-rich kinase (SPAK), upstream regulators of the Na+-K+-2Cl− cotransporter (NKCC1)—essential for spermatogenesis—in mouse models of male fertility. Global OSR1+/− gene mutations, but not global SPAK−/− or Sertoli cell (SC)-specific OSR1 gene knockout (SC-OSR1−/−), cause subfertility with impaired sperm function and are associated with reduced abundance of phosphorylated (p)-NKCC1 but increased p-SPAK expression in testicular tissue and spermatozoa. To dissect further in a SC-specific manner the compensatory effect of OSR1 and SPAK in male fertility, we generated SC-OSR1−/− and SPAK−/− double knockout (DKO) male mice. These are infertile with defective spermatogenesis, presenting a SC-only-like syndrome. Disrupted meiotic progression and increased germ cell apoptosis occurred in the first wave of spermatogenesis. The abundance of total and p-NKCC1 was significantly decreased in the testicular tissues of DKO mice. These results indicate that OSR1 and SPAK cooperatively regulate NKCC1-dependent spermatogenesis in a SC-restricted manner.

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Understanding spermatogenesis is a prerequisite for treatment

Cited by 188 publications

References 29 publications

Sertoli–germ cell junctions in the testis: a review of recent data

Sertoli–germ cell junctions in the testis: a review of recent data

Polydeoxyribonucleotide, an Adenosine-A2A Receptor Agonist, Preserves Blood Testis Barrier from Cadmium-Induced Injury

OSR1 and SPAK cooperatively modulate Sertoli cell support of mouse spermatogenesis

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