Regulation of the blood-testis barrier

Stanton, Peter G.

doi:10.1016/j.semcdb.2016.06.018

Cited by 177 publications

(128 citation statements)

References 111 publications

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“…It has been postulated that these molecules affect the expression and assembly of the junctional proteins, e.g. zonulin/zonula occludens-1 (ZO-1), occludin, claudins and actinmyosin cytoskeletal proteins, thereby induce opening of the cell junctions between the adjacent Sertoli cells and lead to disturbances in the niche of seminiferous epithelium essential for spermatogenesis (Zhang et al 2014, Chojnacka et al 2016, Li et al 2016, Stanton 2016. In fact, impaired BTB and decreased expression of junctional proteins in Sertoli cell have been observed in many obese animal models induced by diet (Liu et al 2014, Fan et al 2015.…”

Section: Obesity Induces Inflammationmentioning

confidence: 99%

Obesity, a serious etiologic factor for male subfertility in modern society

Liu¹,

Ding²

2017

Reproduction

180

141

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Obesity, defined as excessive accumulation of fat in adipose tissue, is a metabolic disorder resulting from behavioral, environmental and heritable causes. Obesity increases the risks of hypertension, diabetes, cardiovascular disease, sleep apnea, respiratory problems, osteoarthritis and cancer. Meanwhile, the negative impact of obesity on male reproduction is gradually recognized. According to the clinical investigations and animal experiments, obesity is correlated with reductions in sperm concentration and motility, increase in sperm DNA damage and changes in reproductive hormones. Several mechanisms can elucidate the effects of obesity on sperm functions and male subfertility, i.e., the excessive conversion of androgens into estrogens in redundant adipose tissue causes sexual hormone imbalance, subsequently resulting in hypogonadism. Secondly, adipokines produced by adipose tissue induce severe inflammation and oxidative stress in male reproductive tract, directly impairing testicular and epididymal tissues. Moreover, increased scrotal adiposity leads to increase gonadal heat, continuously hurting spermatogenesis. Therefore, obesity alters the systematic and regional environment crucial for spermatogenesis in testis and sperm maturation in epididymis, and finally results in poor sperm quality including decreased sperm motility, abnormal sperm morphology and acrosome reaction, changed membrane lipids and increased DNA damage. Furthermore, recent studies indicate that epigenetic changes may be a consequence of increased adiposity. A major effort to identify epigenetic determinants of obesity revealed that sperm DNA methylation and non-coding RNA modification are associated with BMI changes and proposed to inherit metabolic comorbidities across generations. This review will explain how obesity-related changes in males to influence sperm function and male fertility as well.Reproduction (2017) 154 R123-R131

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Section: Obesity Induces Inflammationmentioning

confidence: 99%

Obesity, a serious etiologic factor for male subfertility in modern society

Liu¹,

Ding²

2017

Reproduction

180

141

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“…For instance, the morphological changes in testicular cells observed in those individuals were attributed to the increased permeability of the bloodtestis barrier (BTB). The BTB, composed by adjacent Sertoli cells, assures the unique biochemical milieu required to the occurrence of spermatogenesis (for review Stanton 2016). In fact, male mice fed with a high-fat diet (HFD) for 10 weeks developed obesity and presented an increase in sperm abnormalities with a marked decrease on sperm motility, which were suggested to occur due to severe disruption in BTB and atrophy of the seminiferous epithelia (Fan et al 2015).…”

Section: Obesity and Male Reproduction R179mentioning

confidence: 99%

Obesity, energy balance and spermatogenesis

Oliveira¹,

Sousa²,

Silva³

et al. 2017

Reproduction

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Obesity has grown to pandemic proportions. It affects an increasing number of children, adolescents and young adults exposed to the silent comorbidities of this disorder for a longer period. Infertility has arisen as one important comorbidity associated with the energy dysfunction promoted by obesity. Spermatogenesis is a highly regulated process that is determined by specific energetic requirements. The reproductive potential of males relies on hormonal-dependent and -independent stimuli that control sperm quality. There are conflicting data concerning the impact of male overweight and obesity on sperm quality, as well as on the possible paternal-induced epigenetic trait inheritance of obesity. In addition, it remains a matter of debate whether massive weight loss induced by lifestyle interventions, drugs or bariatric surgery may or may not benefit obese men seeking fatherhood. Herein, we propose to discuss how energy balance may modulate hormonal signalling and sperm quality in overweight and obese men. We also discuss some molecular mechanisms that mediate obesity-related dysfunction in male reproductive system and how paternal obesity may lead to trait inheritance. Finally, we will discuss how lifestyle modifications and sustained weight loss, particularly the loss achieved by bariatric surgery, may revert some of the deleterious effects of obesity in men and their offspring.Reproduction (2017) 153 R173-R185

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“…This barrier is essential, required for the completion of germ cell meiosis and progression into spermiogenesis (Vitale, Fawcett, & Dym, ). BTB integrity is regulated by endocrine (follicle‐stimulating hormone, luteinizing hormone (LH), and androgens) as well as paracrine (TGFB superfamily and retinoid signaling) secretions (Stanton, ). The integrity of the BTB can also be affected by various factors including genetic, environmental toxicants, inflammation, and disease.…”

Section: Testicular Immune Mechanismmentioning

confidence: 99%

Immune regulatory molecules as modifiers of semen and fertility: A review

Archana

Selvaraju

Binsila

et al. 2019

Molecular Reproduction Devel

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Declining fertility rates in both human and animals is a cause for concern. While many of the infertility cases are due to known causes, idiopathic infertility is reported in 30% of the infertile couples. In such cases, 18% of the infertile males carry antisperm antibodies (ASAs). Such data are lacking in livestock, wherein 20–30% of the animals are being culled due to low fertility. In males, the blood–testis barrier (BTB) and biomolecules in the semen provide an immuno‐tolerant microenvironment for spermatozoa as they traverse the immunologic milieu of both the male and female reproductive tracts. For example, insults from environmental contaminants, infections and inflammatory conditions are likely to impact the immune privilege state of the testis and fertility. The female mucosal immune system can recognize allogenic spermatozoa‐specific proteins affecting sperm kinematics and sperm‐zona binding leading to immune infertility. Elucidating the functions and pathways of the immune regulatory molecules associated with fertilization are prerequisites for understanding their impact on fertility. An insight into biomolecules associated with spermatozoal immune tolerance may generate inputs to develop diagnostic tools and modulate fertility. High‐throughput sequencing technologies coupled with bioinformatics analyses provides a path forward to define the array of molecules influencing pregnancy outcome. This review discusses the seminal immune regulatory molecules from their origin in the testis until they traverse the uterine environment enabling fertilization and embryonic development. Well‐designed experiments and the identification of biomarkers may provide a pathway to understand the finer details of reproductive immunology that will afford personalized therapies.

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Regulation of the blood-testis barrier

Cited by 177 publications

References 111 publications

Obesity, a serious etiologic factor for male subfertility in modern society

Obesity, a serious etiologic factor for male subfertility in modern society

Obesity, energy balance and spermatogenesis

Immune regulatory molecules as modifiers of semen and fertility: A review

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