7月19日,，Science雜志在線報(bào)道,，科學(xué)家揭示了食管上皮細(xì)胞（EE）單個(gè)祖細(xì)胞群即可完成EE組織的維持和修復(fù)兩項(xiàng)任務(wù),。
食管上皮細(xì)胞（EE）的疾病，如返流性食管炎和癌癥，發(fā)病率正在上升,。盡管這樣,，EE的穩(wěn)態(tài)維持和修復(fù)的細(xì)胞生物學(xué)仍存在許多爭議。
本研究發(fā)現(xiàn),，在小鼠中,，EE是由單個(gè)細(xì)胞群隨機(jī)分裂生成所維持的。這些祖細(xì)胞以相同的概率分裂產(chǎn)生增殖性的或分化性的子細(xì)胞,。
受到全反式維甲酸（atRA）刺激,，子細(xì)胞命運(yùn)的平衡性仍保持不變，但細(xì)胞分裂的速度增加了,。然而,，受損傷后，細(xì)胞可逆性地轉(zhuǎn)換到生產(chǎn)過量的增殖性子細(xì)胞,，直到傷口愈合,。這種命運(yùn)的開關(guān)，使得單個(gè)的祖細(xì)胞群就能夠行使維持和修復(fù)組織的功能,，而無須"儲備"一個(gè)循環(huán)緩慢的干細(xì)胞池,。(生物谷bioon.com)
doi:10.1016/j.cell.2011.10.017
PMC:
PMID:
A Single Progenitor Population Switches Behavior to Maintain and Repair Esophageal Epithelium
David P. Doupé1,4,*,Maria P. Alcolea1,*,Amit Roshan1,Gen Zhang2,Allon M. Klein2,3,Benjamin D. Simons2,4,Philip H. Jones1,?
Diseases of the esophageal epithelium (EE), such as reflux esophagitis and cancer, are rising in incidence. Despite this, the cellular behaviors underlying EE homeostasis and repair remain controversial. Here, we show that in mice, EE is maintained by a single population of cells that divide stochastically to generate proliferating and differentiating daughters with equal probability. In response to challenge with all-trans retinoic acid (atRA), the balance of daughter cell fate is unaltered, but the rate of cell division increases. However, following wounding, cells reversibly switch to producing an excess of proliferating daughters until the wound has closed. Such fate-switching enables a single progenitor population to both maintain and repair tissue without the need for a “reserve” slow-cycling stem cell pool.
