美國威斯康星州大學(xué)科學(xué)家在《發(fā)育》雜志上撰文說,，他們已經(jīng)成功從人類胚胎干細(xì)胞中培育出了能產(chǎn)生髓磷脂的細(xì)胞，這一發(fā)現(xiàn)為基礎(chǔ)研究和臨床研究開辟了新的前景,。
研究人員培育出的這種細(xì)胞叫少突膠質(zhì)細(xì)胞，它負(fù)責(zé)在中樞神經(jīng)系統(tǒng)中產(chǎn)生髓磷脂,。髓磷脂在神經(jīng)纖維周圍形成絕緣層保護(hù)神經(jīng),，并加快神經(jīng)沖動(dòng)的傳遞。髓磷脂喪失或受到損壞會(huì)產(chǎn)生像多發(fā)性硬化這樣的嚴(yán)重后果,，因?yàn)闆]有髓磷脂神經(jīng)就會(huì)失去相互之間傳遞神經(jīng)沖動(dòng)的能力,，其功能就得不到正常發(fā)揮。
與人類干細(xì)胞不同,，利用小鼠的胚胎干細(xì)胞形成少突膠質(zhì)細(xì)胞相對容易一些,，研究人員經(jīng)常將小鼠的胚胎干細(xì)胞暴露于一種叫Sonic Hedgehog的蛋白里使其在胚胎的脊髓中產(chǎn)生少突膠質(zhì)細(xì)胞。研究人員張?zhí)K春博士和同事證明,，利用人類胚胎干細(xì)胞和這種蛋白也可以產(chǎn)生少突膠質(zhì)細(xì)胞,，只是時(shí)間相對長一些，大約需要14周時(shí)間,，而小鼠只需2周時(shí)間,。此外，兩者之間還有另外一種不同：促使小鼠胚胎干細(xì)胞發(fā)育成少突膠質(zhì)細(xì)胞的生長因子Fgf2實(shí)際上會(huì)延緩人類胚胎干細(xì)胞成為少突膠質(zhì)細(xì)胞的速度,。
張博士說,，這一發(fā)現(xiàn)十分意外，細(xì)胞對同一種因子的反應(yīng)會(huì)有差別，這也許可以解釋為什么過去十年里許多有關(guān)人類神經(jīng)干細(xì)胞培育少突膠質(zhì)細(xì)胞的研究不能成功的原因,。
張博士認(rèn)為這一發(fā)現(xiàn)也具有臨床價(jià)值,。我們現(xiàn)在已經(jīng)可以產(chǎn)生相對豐富的、用來修復(fù)髓鞘的少突膠質(zhì)細(xì)胞的前體細(xì)胞,。通過這一研究發(fā)現(xiàn)也讓我們認(rèn)識到,，在用動(dòng)物研究人類生物學(xué)方面是有差別的。在這一點(diǎn)上,，產(chǎn)生自人類胚胎干細(xì)胞或多能干細(xì)胞的人類少突膠質(zhì)細(xì)胞為將來藥物篩選提供了有用的工具,。（生物谷Bioon.com）
生物谷推薦原始出處：
Development 136, 1443-1452 (2009) doi: 10.1242/10.1242/dev.029447
Human oligodendrocytes from embryonic stem cells: conserved SHH signaling networks and divergent FGF effects
Bao-Yang Hu*, Zhong-Wei Du*, Xue-Jun Li, Melvin Ayala and Su-Chun Zhang
Departments of Anatomy and Neurology, School of Medicine and Public Health, Waisman Center, University of Wisconsin-Madison, 1500 Highland Avenue, Madison, WI 53705, USA.
Human embryonic stem cells (hESCs) offer a platform to bridge what we have learned from animal studies to human biology. Using oligodendrocyte differentiation as a model system, we show that sonic hedgehog (SHH)-dependent sequential activation of the transcription factors OLIG2, NKX2.2 and SOX10 is required for sequential specification of ventral spinal OLIG2-expressing progenitors, pre-oligodendrocyte precursor cells (pre-OPCs) and OPCs from hESC-derived neuroepithelia, indicating that a conserved transcriptional network underlies OPC specification in human as in other vertebrates. However, the transition from pre-OPCs to OPCs is protracted. FGF2, which promotes mouse OPC generation, inhibits the transition of pre-OPCs to OPCs by repressing SHH-dependent co-expression of OLIG2 and NKX2.2. Thus, despite the conservation of a similar transcriptional network across vertebrates, human stem/progenitor cells may respond differently to those of other vertebrates to certain extrinsic factors.
