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首页> 外文期刊>Toxicological sciences: An official journal of the Society of Toxicology >FasL gene-deficient mice display a limited disruption in spermatogenesis and inhibition of mono-(2-ethylhexyl) phthalate-induced germ cell apoptosis.
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FasL gene-deficient mice display a limited disruption in spermatogenesis and inhibition of mono-(2-ethylhexyl) phthalate-induced germ cell apoptosis.

机译：FasL基因缺陷小鼠表现出有限的精子发生破坏和邻苯二甲酸单-（2-乙基己基）酯诱导的生殖细胞凋亡的抑制作用。

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摘要

FasL (TNFSF6, CD95L) is hypothesized to trigger testicular germ cell apoptosis that normally occurs during a distinct peripubertal period as well as in response to toxicant-induced Sertoli cell injury. To test this hypothesis, we evaluated the testis of FasL gene-deficient mice (FasL(-/-)) at two distinct developmental ages (postnatal day [PND] 28 and 44) and after toxicant-induced Sertoli cell injury. Testicular cross sections from peripubertal (PND 28) FasL(-/-) mice showed significant increases in the basal germ cell apoptotic index (AI; 20.58 +/- 4.59) as compared to the testis of C57BL/6J wild-type mice (5.16 +/- 0.08) and closely correlated with increased expression of TRAIL protein in the testis of FasL(-/-) mice. A limited, but significant, number of seminiferous tubules in the testis of PND 28 FasL(-/-) mice showed a severe loss of germ cells with only Sertoli cells present. In contrast, no apparent gross histological changes were observed in the testis of adult (PND 44) FasL(-/-) mice. However, PND 44 FasL(-/-) mice did show a 51% reduction in homogenization-resistant elongate spermatids as compared to age-matched C57BL/6J mice. Exposure of PND 28 FasL(-/-) mice to mono-(2-ethylhexyl) phthalate (MEHP), a well-described Sertoli cell toxicant, unexpectedly caused a rapid decrease in the germ cell AI that paralleled increased levels of the CFLAR (c-FLIP) protein, a known inhibitor of death receptor signaling. In contrast, MEHP treatment did not decrease c-FLIP levels in PND 28 C57BL/6J mice. Taken together, these findings indicate that FasL protein expression is required during the peripubertal period for the proper regulation of germ cell apoptosis that occurs normally during this period. The influence of FasL on the cellular regulation of c-FLIP protein levels appears to be a unique mechanism for modulating germ cell apoptosis after toxicant-induced Sertoli cell injury.
机译：假定FasL（TNFSF6，CD95L）会触发睾丸生殖细胞凋亡，这通常发生在青春期不同的时期，以及对有毒物引起的Sertoli细胞损伤的反应。为了验证该假设，我们评估了FasL基因缺陷小鼠（FasL（-/-））在两个不同的发育年龄（出生后[PND] 28和44日）以及有毒物诱导的Sertoli细胞损伤后的睾丸。与C57BL / 6J野生型小鼠的睾丸相比，青春期（PND 28）FasL（-/-）小鼠的睾丸横截面显示基础生殖细胞凋亡指数（AI; 20.58 +/- 4.59）显着增加+/- 0.08），并与FasL（-/-）小鼠睾丸中TRAIL蛋白表达的增加密切相关。 PND 28 FasL（-/-）小鼠睾丸中的精小管数量有限，但意义重大，显示仅存在支持细胞的生殖细胞严重丧失。相反，在成年（PND 44）FasL（-/-）小鼠的睾丸中未观察到明显的组织学变化。但是，与年龄匹配的C57BL / 6J小鼠相比，PND 44 FasL（-/-）小鼠确实显示出抗均质性的细长精子细胞减少51％。 PND 28 FasL（-/-）小鼠暴露于邻苯二甲酸单-（2-乙基己基）酯（MEHP）（一种描述良好的Sertoli细胞毒物），出乎意料地导致了生殖细胞AI的迅速下降，与CFLAR的水平升高平行（ c-FLIP）蛋白，一种已知的死亡受体信号传导抑制剂。相反，MEHP处理并未降低PND 28 C57BL / 6J小鼠的c-FLIP水平。综上所述，这些发现表明在青春期期间需要FasL蛋白表达，以正常调节在此期间正常发生的生殖细胞凋亡。 FasL对c-FLIP蛋白水平的细胞调节的影响似乎是有毒物诱导的Sertoli细胞损伤后调节生殖细胞凋亡的独特机制。

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