Testicular Annexin A5 Expression Augmented by Experimental Cryptorchidism and Could Affect Germ Cell Apoptosis in Rats

Yao, Bing; Rieanrakwong, Duangjai; Kawaminami, Mitsumori

doi:10.1016/j.urology.2008.11.021

Cited by 7 publications

(4 citation statements)

References 20 publications

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“…5B ). The appearance of TUNEL-positive cells was always accompanied by augmented Annexin V expression 20 , which can recognize and clear apoptotic cells 21 . As expected, a high Annexin V level was observed in the BRD7 −/− mice testes, as detected by western blotting ( Fig.…”

Section: Resultsmentioning

confidence: 98%

Knockout of BRD7 results in impaired spermatogenesis and male infertility

Wang

Zhao

Guo

et al. 2016

Sci Rep

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BRD7 was originally identified as a novel bromodomain gene and a potential transcriptional factor. BRD7 was found to be extensively expressed in multiple mouse tissues but was highly expressed in the testis. Furthermore, BRD7 was located in germ cells during multiple stages of spermatogenesis, ranging from the pachytene to the round spermatid stage. Homozygous knockout of BRD7 (BRD7−/−) resulted in complete male infertility and spermatogenesis defects, including deformed acrosomal formation, degenerative elongating spermatids and irregular head morphology in postmeiotic germ cells in the seminiferous epithelium, which led to the complete arrest of spermatogenesis at step 13. Moreover, a high ratio of apoptosis was determined by TUNEL analysis, which was supported by high levels of the apoptosis markers annexin V and p53 in knockout testes. Increased expression of the DNA damage maker λH2AX was also found in BRD7−/− mice, whereas DNA damage repair genes were down−regulated. Furthermore, no or lower expression of BRD7 was detected in the testes of azoospermia patients exhibiting spermatogenesis arrest than that in control group. These data demonstrate that BRD7 is involved in male infertility and spermatogenesis in mice, and BRD7 defect might be associated with the occurrence and development of human azoospermia.

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Section: Resultsmentioning

confidence: 98%

Knockout of BRD7 results in impaired spermatogenesis and male infertility

Wang

Zhao

Guo

et al. 2016

Sci Rep

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“…The altered expression of genes regulated by FSH and LH pathway was found. The up-regulation of INHBA and ANXA5 affects the FSH level and the hypotalamo-pitutitary axis respectively, regulating the testosterone production4243. Thirty-one down-modulated transcripts participate in the regulation of “Endocrine system disorders” (Fig.…”

Section: Discussionmentioning

confidence: 99%

Testis Transcriptome Modulation in Klinefelter Patients with Hypospermatogenesis

D’Aurora

Ferlin

Garolla

et al. 2017

Sci Rep

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The main genetic cause of male infertility is represented by the Klinefelter Syndrome (KS), a condition accounting for 3% of all cases of infertility and up to15% of cases of azoospermia. KS is generally characterized by azoospermia; approximately 10% of cases have severe oligozoospermia. Among these, the 30–40% of patients show hypospermatogenesis. The mechanisms leading to adult testis dysfunctions are not completely understood. A microarray transcriptome analysis was performed on testis biopsies obtained from three KS patients with hypospermatogenesis and three control subjects. KS testis showed a differential up- and down-regulation of 303 and 747 transcripts, respectively, as compared to controls. The majority of down-regulated transcripts were involved in spermiogenesis failure and testis morphological defects, whereas up-regulated genes were responsible for testis apoptotic processes. Functional analysis of the transcriptionally altered genes indicated a deregulation in cell death, germ cell function and morphology as well as blood-testis-barrier maintenance and Leydig cells activity. These data support a complex scenario in which spermatogenic impairment is the result of functional and morphological alterations in both germinal and somatic components of KS testis. These findings could represent the basis for evaluating new markers of KS spermatogenesis and potential targets of therapeutic intervention to preserve residual spermatogenesis.

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“…ANXA1 and ANXA5 are important mediator of the hypotalamo-pitutitary axis, regulating testosterone production. The effect of their over-expression, observed in KS testis, could be related to LCs dysfunction resulting in LCs death [26,27]. StAR, SCARB1, CAV1 and CAV2 mediate the traffiking of cholesterol, essential to begin the synthesis of pregnenolone.…”

Section: Discussionmentioning

confidence: 99%

Deregulation of sertoli and leydig cells function in patients with klinefelter syndrome as evidenced by testis transcriptome analysis

et al. 2015

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BackgroundKlinefelter Syndrome (KS) is the most common abnormality of sex chromosomes (47,XXY) and represents the first genetic cause of male infertility. Mechanisms leading to KS testis degeneration are still not completely defined but considered to be mainly the result of germ cells loss. In order to unravel the molecular basis of global testis dysfunction in KS patients, we performed a transcriptome analysis on testis biopsies obtained from 6 azoospermic non-mosaic KS patients and 3 control subjects.ResultsThe analysis found that, compared to controls, KS patients showed the differential up- and down-expression of 656 and 247 transcripts. The large majority of the deregulated transcripts were expressed by Sertoli cells (SCs) and Leydig cells (LCs). Functional analysis of the deregulated transcripts indicated changes of genes involved in cell death, inflammatory response, lipid metabolism, steroidogenesis, blood-testis-barrier formation and maintenance, as well as spermatogenesis failure.ConclusionsTaken together, present data highlight the modulation of hundreds of genes in the somatic components of KS patient testis. The increased LCs steroidogenic function together with the impairment of inflammatory pathways and BTB structure, result in increased apoptosis. These findings may represent a critical roadmap for therapeutic intervention and prevention of KS-related testis failure.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1356-0) contains supplementary material, which is available to authorized users.

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Testicular Annexin A5 Expression Augmented by Experimental Cryptorchidism and Could Affect Germ Cell Apoptosis in Rats

Cited by 7 publications

References 20 publications

Knockout of BRD7 results in impaired spermatogenesis and male infertility

Knockout of BRD7 results in impaired spermatogenesis and male infertility

Testis Transcriptome Modulation in Klinefelter Patients with Hypospermatogenesis

Deregulation of sertoli and leydig cells function in patients with klinefelter syndrome as evidenced by testis transcriptome analysis

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