日本一个研究小组在新一期美国《国家科学院学报》网络版上报告说，他们利用无法产生精子的实验鼠的精巢组织，成功获得了正常精子。
这些精巢无法生成精子的实验鼠是横滨市立大学研究人员通过基因操作手法获得的，它们的精巢内虽然有能够发育成精子的精原细胞，但是向精原细胞提供营养、促进其成熟的支柱细胞不能发挥作用，从而无法生成精子。
研究人员摘取这种实验鼠精巢的组织样本，并添加能够促进精子成熟的“KITL”蛋白质等物质加以培养，结果获得了正常精子。利用这些精子进行人工授精后产出了正常的老鼠。研究人员指出，这一成果还无法直接应用于人类，但理论上，若能实现男性不育症患者精巢组织的体外培养，有可能促进精子的形成。（生物谷Bioon.com）
doi: 10.1073/pnas.1211845109
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Testis tissue explantation cures spermatogenic failure in c-Kit ligand mutant mice
Takuya Sato, Tetsuhiro Yokonishi, Mitsuru Komeya, Kumiko Katagiri, Yoshinobu Kubota, Shogo Matoba, Narumi Ogonuki, Atsuo Ogura, Shosei Yoshida, and Takehiko Ogawa
Male infertility is most commonly caused by spermatogenic defects or insufficiencies, the majority of which are as yet cureless. Recently, we succeeded in cultivating mouse testicular tissues for producing fertile sperm from spermatogonial stem cells. Here, we show that one of the most severe types of spermatogenic defect mutant can be treated by the culture method without any genetic manipulations. The Sl/Sld mouse is used as a model of such male infertility. The testis of the Sl/Sld mouse has only primitive spermatogonia as germ cells, lacking any sign of spermatogenesis owing to mutations of the c-kit ligand (KITL) gene that cause the loss of membrane-bound-type KITL from the surface of Sertoli cells. To compensate for the deficit, we cultured testis tissues of Sl/Sld mice with a medium containing recombinant KITL and found that it induced the differentiation of spermatogonia up to the end of meiosis. We further discovered that colony stimulating factor-1 (CSF-1) enhances the effect of KITL and promotes spermatogenesis up to the production of sperm. Microinsemination of haploid cells resulted in delivery of healthy offspring. This study demonstrated that spermatogenic impairments can be treated in vitro with the supplementation of certain factors or substances that are insufficient in the original testes.
