Male germ cell death in mouse testes: Possible involvement of Fas and Fas ligand

Male germ cell death in mouse testes: Possible involvement of Fas and Fas ligand
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DOI:
10.1007/s007950100018
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发表时间:
2001-12-01
期刊:
Medical Electron Microscopy
影响因子:
--
通讯作者:
Koji, Takehiko
Koji, Takehiko
中科院分区:
其他
文献类型:
--
作者:
Koji, Takehiko

文献摘要

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在哺乳动物精子发生的各个阶段,生殖细胞的丢失是非常常见的。虽然细胞死亡,特别是细胞凋亡,已牵连,我们的了解生殖细胞死亡的机制仍然有限。为了阐明生殖细胞死亡的程度和机制,这篇综述首先涵盖了什么是已知的胚胎,新生儿和成年小鼠的正常睾丸从电子显微镜(EM)和末端dUTP缺口末端标记(TUNEL)染色的生殖细胞变性。Fas和Fas配体(FasL)系统是否参与诱导生殖细胞凋亡在正常和受损的睾丸的问题,然后解决,包括考虑缺血-再灌注模型的睾丸扭转和雌激素处理的睾丸模型的环境内分泌干扰。最后,本文提出,不同的分子途径可能会触发诱导雄性生殖细胞凋亡,这取决于生殖细胞的生理和病理状态。
Loss of germ cells is very common during various stages of mammalian spermatogenesis. Although cell death, particularly apoptosis, has been implicated, our understanding of the mechanisms underlying germ cell death is still limited. In order to elucidate the extent and mechanism of germ cell death, this review first covers what is known of germ cell degeneration in the normal testes of fetal, neonatal, and adult mice from electron microscopy (EM) and from terminal dUTP nick-end labeling (TUNEL) staining. The issue of whether the Fas and Fas ligand (FasL) system is involved in the induction of germ cell apoptosis in normal and damaged testes is then addressed, including consideration of both the ischemia-reperfusion model of testicular torsion and the estrogen-treated testis model of environmental endocrine disruption. Finally, this review proposes that different molecular pathways may be triggered to induce male germ cell apoptosis, depending upon the physiological and pathological states of the germ cells.