Spermatogonial proliferation and apoptosis in hypospermatogenesis associated with nonobstructive azoospermia

Takagi, Seiji; Itoh, Naoki; Kimura, Makoto; Sasao, Takumi; Tsukamoto, Taiji

doi:10.1016/s0015-0282(01)02732-7

Cited by 60 publications

(55 citation statements)

References 25 publications

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“…Of note, in cases of Hyp, which is the most heterogenous group (Takagi et al 2001), we could identify both groups of patients with high or low efficiency of meiosis in almost all combinations with reduced numbers of early spermatogonia or reduced numbers of dividing/differentiating spermatogonia. However, in contrast to cases with MA, the frequency of low efficiency of meiosis was clearly lower in cases of Hyp.…”

Section: Discussionmentioning

confidence: 90%

“…Especially in patients with maturation arrest (MA) a significant reduction in dividing spermatogonia during mitosis was observed (Steger et al 1998, Bar-Shira Maymon et al 2003, whereas in hypospermatogenesis (Hyp)-accelerated apoptosis rather than proliferative dysfunction was suggested to be responsible for reduced spermatogonial cell numbers (Takagi et al 2001). In addition, in cases with MA reduced recombination rates (up to 50%) were found (Gonsalves et al 2004, Egozcue et al 2005 and an increased frequency of genetic abnormalities (Weedin et al 2011).…”

Section: Introductionmentioning

confidence: 99%

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Role of compensatory meiosis mechanisms in human spermatogenesis

Borgers¹,

Wolter²,

Hentrich³

et al. 2014

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Disturbances of checkpoints in distinct stages of spermatogenesis (mitosis, meiosis, and spermiogenesis) contribute to impaired spermatogenesis; however, the efficiency of meiotic entry has not been investigated in more detail. In this study, we analyzed azoospermic patients with defined spermatogenic defects by the use of octamer-binding protein 2 for type A spermatogonia, sarcoma antigen 1 for mitosis-meiosis transition and SMAD3 for pachytene spermatocytes. Especially patients with maturation arrest (MA) at the level of primary spermatocytes showed significantly reduced numbers of spermatogonia compared with patients with histologically intact spermatogenesis or patients with hypospermatogenesis (Hyp). For a detailed individual classification of the patients, we distinguished between 'high efficiency of meiotic entry' (high numbers of pachytene spermatocytes) and 'low efficiency of meiotic entry' (low numbers of pachytene spermatocytes). Only patients with histologically normal spermatogenesis (Nsp) and patients with Hyp showed normal numbers of spermatogonia and a high efficiency of meiotic entry. Of note, only patients with histologically Nsp or patients with Hyp could compensate low numbers of spermatogonia with a high efficiency of meiotic entry. In contrast, patients with MA always showed a low efficiency of meiotic entry. This is the first report on patients with impaired spermatogenesis, showing that half of the patients with Hyp but all patients with MA cannot compensate reduced numbers in spermatogonia with a highly efficient meiosis. Thus, we suggest that compensatory meiosis mechanisms in human spermatogenesis exist.

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Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Role of compensatory meiosis mechanisms in human spermatogenesis

Borgers¹,

Wolter²,

Hentrich³

et al. 2014

Reproduction

View full text Add to dashboard Cite

show abstract

“…In the face of DNA damage and possibly of low levels of DNA repair, apoptosis may be the process of last resort to ensure against transmission of DNA defects to the embryo. Overexpression of apoptotic events in germ cells could lead to oligozoospermia or azoospermia and thus infertility (102,103). Conversely, underexpression of apoptotic events will lead to survival and thus fertilization by sperm with faulty DNA (73), potentially resulting in early embryonic loss or unhealthy offspring (104).…”

Section: Discussionmentioning

confidence: 99%

Effects of age on DNA double-strand breaks and apoptosis in human sperm

Singh

Müller

Berger

2003

Fertility and Sterility

395

223

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“…Nodera et al [2001] also reported the appearance of TUNEL positive cells after 3 w of zinc deficiency in testes and thymus of 7 w old Sprague Dawley rats. Abnormally accelerated apoptosis of germ cells may lead to an imbalance of cell proliferation and death resulting in spermatogenic impairment [Takagi et al 2001;Kimura et al 2003]. The correct balance between the apoptotic pathways is important for the maintenance of genomic integrity while preventing unnecessary cell death [Clarke and Allan 2009].…”

Section: Groupsmentioning

confidence: 99%