據(jù)物理學(xué)家組織網(wǎng)近日報(bào)道，美國科學(xué)家采用一種新奇的方法,，對誘導(dǎo)多能干細(xì)胞（iPS細(xì)胞）進(jìn)行分化,，在試管內(nèi)制造出了無數(shù)的人類紅血細(xì)胞和血小板。他們表示,，得到的紅血細(xì)胞有望用于診查瘧疾和鐮狀細(xì)胞血癥,，而血小板則可用來探查心血管病并治療凝血障礙。研究發(fā)表在最新一期的《血液》雜志上,。
科學(xué)家們一般通過對成人干細(xì)胞進(jìn)行重組,，讓其回到初始的干細(xì)胞狀態(tài),，從而獲得iPS細(xì)胞。iPS細(xì)胞可以利用皮膚細(xì)胞,、血液細(xì)胞等成熟的身體細(xì)胞生成,，并可進(jìn)一步分化成各種其他類型的細(xì)胞。由于其源于病人體內(nèi),，不會(huì)引發(fā)免疫排斥反應(yīng),，從而成為生物研究領(lǐng)域的一個(gè)強(qiáng)大工具以及再生醫(yī)療的重要來源。
最新研究中用到的iPS細(xì)胞來自波士頓大學(xué)再生醫(yī)學(xué)中心的誘導(dǎo)多能干細(xì)胞庫,。該中心聯(lián)合負(fù)責(zé)人兼波士頓大學(xué)醫(yī)學(xué)院助理教授喬治·墨菲與波士頓大學(xué)公共健康學(xué)院環(huán)境健康教授戴維·希爾攜手領(lǐng)導(dǎo)的研究團(tuán)隊(duì)首先讓這些iPS細(xì)胞接觸生長因子,，隨后用一種專利技術(shù)誘導(dǎo)它們分化成了紅血細(xì)胞和血小板?？茖W(xué)家們也對iPS細(xì)胞進(jìn)行了深入診查,，以研究血液細(xì)胞如何形成以及這一過程在身體內(nèi)如何被調(diào)節(jié)。
該研究的新奇之處是研究人員在其中添加了用來調(diào)節(jié)芳香烴受體（AhR）通路的化合物,。以前的研究表明,，這一通路會(huì)通過芳香烴受體同環(huán)境中的有毒物質(zhì)相互作用來促進(jìn)癌細(xì)胞發(fā)育。然而,，在最新研究中,，功能性紅血細(xì)胞和血小板的產(chǎn)量在短時(shí)間內(nèi)呈指數(shù)增加，這表明,，AhR在正常的血液細(xì)胞的發(fā)育過程中也起重要作用,。
墨菲說：“最新發(fā)現(xiàn)使我們獲得了大量的紅血細(xì)胞和血小板，可以滿足治療所需,。而且最新研究也表明,，AhR在血液細(xì)胞如何形成方面具有非常重要的生物學(xué)功能。”
輸血是一種不可缺少的細(xì)胞療法,，血供應(yīng)的安全性和充足性也一直備受關(guān)注,。去年，美國馬里蘭州負(fù)責(zé)統(tǒng)計(jì)血液供應(yīng)和需求的國家血液資源中心報(bào)告稱,，美國的血液供應(yīng)因需求大大超過供給而趨于干涸,，許多州已嚴(yán)重缺血。一些地區(qū)的紅十字會(huì)官員說,，血液嚴(yán)重短缺迫使非急診手術(shù)延期,。墨菲表示：“用病人自己的iPS細(xì)胞生成的紅血細(xì)胞和血小板有望解決與免疫排斥和污染有關(guān)的問題，也有望減少可預(yù)見的血液短缺和獻(xiàn)血需求,。”（生物谷 Bioon.com）
生物谷推薦的英文摘要
Blood doi: 10.1182/blood-2012-11-466722
The aryl hydrocarbon receptor directs hematopoietic progenitor cell expansion and differentiation
Brenden W. Smith1, Sarah S. Rozelle, Amy Leung, Jessalyn Ubellacker, Ashley Parks, Shirley K. Nah, Deborah French, Paul Gadue, Stefano Monti, David H.K. Chui, Martin H. Steinberg, Andrew L. Frelinger, Alan D. Michelson6, Roger Theberge, Mark E. McComb, Catherine E. Costello, Darrell N. Kotton, Gustavo Mostoslavsky, David H. Sherr, and George J. Murphy,*
The evolutionarily conserved aryl hydrocarbon receptor (AhR) has been studied for its role in environmental chemical-induced toxicity. However, recent studies demonstrate that the AhR may regulate the hematopoietic and immune systems during development in a cell-specific manner. These results, together with the absence of an in vitro model system enabling production of large numbers of primary human hematopoietic progenitor cells (HPs) capable of differentiating into megakaryocyte- and erythroid-lineage cells, motivated us to determine if AhR modulation could facilitate both progenitor cell expansion and megakaryocyte and erythroid cell differentiation. Using a novel, iPSC-based, chemically-defined, serum and feeder cell-free culture system, we show that a functional AhR is expressed in HPs, and that remarkably, AhR activation in these HPs drives an unprecedented expansion of HPs, megakaryocyte- and erythroid-lineage cells. Further AhR modulation within rapidly expanding progenitor cell populations directs cell fate, with chronic AhR agonism permissive to erythroid differentiation and acute antagonism favoring megakaryocyte specification. These results highlight the development of a new, GMP-compliant platform for generating virtually unlimited numbers of human HPs with which to scrutinize red blood cell and platelet development, including the assessment of the role of this environmental chemical receptor in critical cell fate decisions during hematopoiesis.
