日前,，美國科學(xué)家最新一項研究表明,，衰老期老鼠和青年期老鼠的血液融合在一起,，能夠起到恢復(fù)活力的作用,，有望使衰老期老鼠獲得新生,。
這支研究小組是由美國馬薩諸塞州哈佛干細(xì)胞協(xié)會艾米-瓦格斯(Amy Wagers)領(lǐng)導(dǎo)的,，他們發(fā)現(xiàn)青年期老鼠的血液好像可以使衰老期老鼠骨髓中衰老的血液干細(xì)胞恢復(fù)活力，同時它也可以恢復(fù)骨髓中一種“生態(tài)區(qū)位細(xì)胞”,，該細(xì)胞起到滋育,、供給和刺激血液干細(xì)胞的作用,。
雖然衰老期老鼠比青年期老鼠體內(nèi)具有更多的血液干細(xì)胞和生態(tài)區(qū)位細(xì)胞，但多數(shù)存在著缺陷,，并且無法像青年期老鼠那樣有效地修復(fù)身體,。艾米說：“衰老期老鼠體內(nèi)有過多的血液干細(xì)胞，很可能是為了彌補血液干細(xì)胞的缺陷,，同時,，衰老期老鼠也有更多的骨髓血細(xì)胞，它很容易引起感染并誘發(fā)癌癥,，此外由于過少的淋巴樣血細(xì)胞,，不能有效地進(jìn)行組織修復(fù)。”
但是當(dāng)研究小組將21個月老鼠體內(nèi)細(xì)胞植入僅2個月的老鼠體內(nèi),，所有相關(guān)年齡狀態(tài)的變化都顛倒了,，血液混合后的老鼠具有很少的骨髓細(xì)胞和更多的淋巴林細(xì)胞。他們指出,，這些青年期老鼠體內(nèi)的血液注入衰老期老鼠體內(nèi),，有望使其變得更加年輕。
著眼于未來更多的實驗,，艾米猜測通過導(dǎo)入1號胰島素樣生長因子(IGF-1),，這種血液成分可能快速修補衰老期老鼠衰老的細(xì)胞，IGF-1因子與身體衰老有著直接關(guān)系,。研究小組猜測IGF-1因子能夠加速老鼠體內(nèi)生態(tài)區(qū)位細(xì)胞的老化進(jìn)程,。當(dāng)研究人員對衰老期老鼠骨髓中注入抵消IGF-1因子的抗體，生態(tài)區(qū)位細(xì)胞和干細(xì)胞將保持年輕狀態(tài),。
艾米指出,，目前這種方法尚處于初級研制階段，它并不是十分安全的,，通過向老年人體內(nèi)骨髓注入抗體可以抵消IGF-1因子,。這是由于IGF-1因子對于肌肉和骨骼生長至關(guān)重要，而抗體可以消除身體內(nèi)剩余的IGF-1因子,。艾米帶領(lǐng)的研究小組目前正在尋求阻止骨髓中IGF-1因子產(chǎn)量啟動化學(xué)信號的方法,。
艾米稱，我們嘗試使用對年輕人進(jìn)行輸血法來延緩衰老,，更加直接地模擬老鼠實驗結(jié)果,。一次性地關(guān)于血液因子實驗并不會產(chǎn)生抗衰老作用，這將是一個持續(xù)性過程,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 463, 495-500 (28 January 2010) | doi:10.1038/nature08749
Systemic signals regulate ageing and rejuvenation of blood stem cell niches
Shane R. Mayack1, Jennifer L. Shadrach1, Francis S. Kim1 & Amy J. Wagers1
1 Department of Stem Cell and Regenerative Biology, Harvard University, Howard Hughes Medical Institute, Harvard Stem Cell Institute, Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts 02115, USA
Ageing in multicellular organisms typically involves a progressive decline in cell replacement and repair processes, resulting in several physiological deficiencies, including inefficient muscle repair, reduced bone mass, and dysregulation of blood formation (haematopoiesis). Although defects in tissue-resident stem cells clearly contribute to these phenotypes, it is unclear to what extent they reflect stem cell intrinsic alterations or age-related changes in the stem cell supportive microenvironment, or niche. Here, using complementary in vivo and in vitro heterochronic models, we show that age-associated changes in stem cell supportive niche cells deregulate normal haematopoiesis by causing haematopoietic stem cell dysfunction. Furthermore, we find that age-dependent defects in niche cells are systemically regulated and can be reversed by exposure to a young circulation or by neutralization of the conserved longevity regulator, insulin-like growth factor-1, in the marrow microenvironment. Together, these results show a new and critical role for local and systemic factors in signalling age-related haematopoietic decline, and highlight a new model in which blood-borne factors in aged animals act through local niche cells to induce age-dependent disruption of stem cell function.
