日本一個研究小組在新一期美國《國家科學(xué)院學(xué)報》（PNAS）網(wǎng)絡(luò)版上報告說，他們利用無法產(chǎn)生精子的實(shí)驗(yàn)鼠的精巢組織,，成功獲得了正常精子,。
這些精巢無法生成精子的實(shí)驗(yàn)鼠是橫濱市立大學(xué)研究人員通過基因操作手法獲得的,，它們的精巢內(nèi)雖然有能夠發(fā)育成精子的精原細(xì)胞，但是向精原細(xì)胞提供營養(yǎng),、促進(jìn)其成熟的支柱細(xì)胞不能發(fā)揮作用,，從而無法生成精子。
研究人員摘取這種實(shí)驗(yàn)鼠精巢的組織樣本,，并添加能夠促進(jìn)精子成熟的“KITL”蛋白質(zhì)等物質(zhì)加以培養(yǎng),，結(jié)果獲得了正常精子。利用這些精子進(jìn)行人工授精后產(chǎn)出了正常的老鼠,。
研究人員指出,，這一成果還無法直接應(yīng)用于人類，但理論上,，若能實(shí)現(xiàn)男性不育癥患者精巢組織的體外培養(yǎng),，有可能促進(jìn)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 Satoa, Tetsuhiro Yokonishia, Mitsuru Komeyaa, Kumiko Katagiria, Yoshinobu Kubotaa, Shogo Matobab, Narumi Ogonukib, Atsuo Ogurab, Shosei Yoshidac,d, and Takehiko Ogawaa,e,f,1
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.
