華盛頓大學(xué)的科學(xué)家首次成功讓活老鼠再生出視網(wǎng)膜細(xì)胞，這為人類再生眼睛細(xì)胞提供了成功的希望,，從而可望恢復(fù)一些盲人的視力,。此研究成果發(fā)表在11月24日出版的美國《國家科學(xué)院院刊》（PNAS）上。
視網(wǎng)膜位于眼睛后面,，其功能是將光線通過神經(jīng)脈沖傳輸?shù)酱竽X中,。先前的研究工作表明視網(wǎng)膜神經(jīng)細(xì)胞（Müller細(xì)胞）可以在培養(yǎng)皿里培育出來。華盛頓大學(xué)的湯姆·李何說：“這種細(xì)胞存在于所有脊椎動物的所有視網(wǎng)膜中,，因此細(xì)胞再生之源也呈現(xiàn)在人類視網(wǎng)膜中,。”科學(xué)家將進(jìn)一步研究治療因視網(wǎng)膜損壞導(dǎo)致失明的辦法。李何表示鳥類像哺乳動物一樣是溫血動物,，它們再生視網(wǎng)膜細(xì)胞的能力有限,，而魚類是冷血動物，能再生所有種類的視網(wǎng)膜細(xì)胞,。
讓老鼠再生視網(wǎng)膜細(xì)胞被認(rèn)為是人類生物學(xué)的理想模式,，但做到這一點(diǎn)并不容易,。研究人員將物質(zhì)注入到視網(wǎng)膜中,，以去除神經(jīng)節(jié)細(xì)胞（一種存在于視網(wǎng)膜表面附近的神經(jīng)細(xì)胞）和無長突細(xì)胞。之后將纖維原細(xì)胞生長因子,、表皮生長因子和胰島素之類的藥物注射到眼睛里,，就能刺激視網(wǎng)膜神經(jīng)細(xì)胞重新開始分裂和增生,，有一些變成了成熟的神經(jīng)細(xì)胞，包括無長突細(xì)胞,。李何說，無長突細(xì)胞能調(diào)節(jié)感光器的電信號,，對眼睛探知運(yùn)動和夜視非常重要,。
然而,，研究人員發(fā)現(xiàn)許多由視網(wǎng)膜神經(jīng)細(xì)胞分裂和增生的原細(xì)胞在形成的第一周之內(nèi)就死亡了,，然而設(shè)法轉(zhuǎn)換成無長突細(xì)胞的這些細(xì)胞至少生存了30天,?？茖W(xué)家對此現(xiàn)象還不清楚是怎么回事。李何說：“我們雖然沒有獲得大量的新神經(jīng)細(xì)胞,，但我們能獲得新的無長突細(xì)胞。”
科學(xué)家表示,，外層的視網(wǎng)膜就像電腦的CPU,，內(nèi)層視網(wǎng)膜像主板,，如果給一塊壞死的主板換上新的CPU,，無論此CPU品質(zhì)如何高，都將無濟(jì)于事,。而再生視網(wǎng)膜細(xì)胞就能很好地解決這一問題,。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS，doi:10.1073/pnas.0807453105,，Mike O. Karl,， Thomas A. Reh
Stimulation of neural regeneration in the mouse retina
Mike O. Karla, Susan Hayesa, Branden R. Nelsona, Kristine Tana, Brian Buckinghamb, and Thomas A. Reha,1
aDepartment of Biological Structure, and
bMedical Science Training Program, 357420 Health Science Center, University of Washington, School of Medicine, Seattle, WA 98195
Abstract
Müller glia can serve as a source of new neurons after retinal damage in both fish and birds. Investigations of regeneration in the mammalian retina in vitro have provided some evidence that Müller glia can proliferate after retinal damage and generate new rods; however, the evidence that this occurs in vivo is not conclusive. We have investigated whether Müller glia have the potential to generate neurons in the mouse retina in vivo by eliminating ganglion and amacrine cells with intraocular NMDA injections and stimulating Müller glial to re-enter the mitotic cycle by treatment with specific growth factors. The proliferating Müller glia dedifferentiate and a subset of these cells differentiated into amacrine cells, as defined by the expression of amacrine cell-specific markers Calretinin, NeuN, Prox1, and GAD67-GFP. These results show for the first time that the mammalian retina has the potential to regenerate inner retinal neurons in vivo.
