一种能够让未成熟的精子细胞过早逃离睾丸的化合物或许为避孕药提供了新的线索。
通过关闭睾丸所独有的基因和蛋白质，那些从事“男性避孕药”研究的科学家最近发现了许多能够阻碍精子生成的方法。
如今，由美国纽约市人口理事会生物医学研究中心的C. Yan Cheng率领的一个研究小组发现了一种阻碍精子发生的新途径：破坏血液—睾丸屏障——这是睾丸与血液循环之间的一道细胞防火墙。
当Cheng的研究小组向小鼠的睾丸中注入一种特殊的蛋白质片段后，血液—睾丸屏障便被瓦解了。
这导致未成熟的精子在它们有能力让卵子受精之前就过早地离开了睾丸。
更重要的是，这些变化是可逆的。研究人员在11月13日的《自然—通讯》网络版上报告了他们的研究成果。
任何潜在的男性避孕药都需要许多年的验证，并经历许多的测试。
例如，Cheng的研究小组并没有测试小鼠爸爸在注入了这种蛋白质片段后是否会有更少的后代。
但Cheng表示，与其他潜在的避孕药相比，这种蛋白质的优势在于它能够被生物体自然而少量地生成，从而可能具有良好的耐受性。（生物谷Bioon.com）
doi:10.1038/ncomms2171
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PMID:
A peptide derived from laminin-γ3 reversibly impairs spermatogenesis in rats
Linlin Su, Dolores D. Mruk, Pearl P.Y. Lie, Bruno Silvestrini & C. Yan Cheng
Cellular events that occur across the seminiferous epithelium in the mammalian testis during spermatogenesis are tightly coordinated by biologically active peptides released from laminin chains. Laminin-γ3 domain IV is released at the apical ectoplasmic specialization during spermiation and mediates restructuring of the blood–testis barrier, which facilitates the transit of preleptotene spermatocytes. Here we determine the biologically active domain in laminin-γ3 domain IV, which we designate F5 peptide, and show that the overexpression of this domain, or the use of a synthetic F5 peptide, in Sertoli cells with an established functional blood–testis barrier reversibly perturbs blood–testis barrier integrity in vitro and in the rat testis in vivo. This effect is mediated via changes in protein distribution at the Sertoli and Sertoli–germ–cell cell interface and by phosphorylation of focal adhesion kinase at Tyr407. The consequences are perturbed organization of actin filaments in Sertoli cells, disruption of the blood–testis barrier and spermatid loss. The impairment of spermatogenesis suggests that this laminin peptide fragment may serve as a contraceptive in male rats.
