Division of Pulmonary, Allergy and Critical Care, Duke University Medical Center, Durham, North Carolina, USA.
Am J Respir Cell Mol Biol. 2011 Jun;44(6):794-803. doi: 10.1165/rcmb.2010-0098OC. Epub 2010 Jul 23.
Air spaces of the mammalian lung are lined by a specialized epithelium that is maintained by endogenous progenitor cells. Within bronchioles, the abundance and distribution of progenitor cells that contribute to epithelial homeostasis change as a function of maintenance versus repair. It is unclear whether functionally distinct progenitor pools or a single progenitor cell type maintain the epithelium and how the behavior is regulated in normal or disease states. To address these questions, we applied fractionation methods for the enrichment of distal airway progenitors. We show that bronchiolar progenitor cells can be subdivided into two functionally distinct populations that differ in their susceptibility to injury and contribution to repair. The proliferative capacity of these progenitors is confirmed in a novel in vitro assay. We show that both populations give rise to colonies with a similar dependence on stromal cell interactions and regulation by TGF-β. These findings provide additional insights into mechanisms of epithelial remodeling in the setting of chronic lung disease and offer hope that pharmacologic interventions may be developed to mitigate tissue remodeling.
哺乳动物肺部的气腔由一种特殊的上皮细胞组成,这种上皮细胞由内源性祖细胞维持。在细支气管中,参与上皮细胞稳态的祖细胞的丰度和分布随着维持和修复的功能而变化。目前尚不清楚是功能不同的祖细胞池还是单一的祖细胞类型维持着上皮细胞,以及在正常或疾病状态下这种行为是如何被调控的。为了解决这些问题,我们应用了分离方法来富集远端气道祖细胞。我们发现,细支气管祖细胞可以细分为两个功能不同的群体,它们在对损伤的敏感性和对修复的贡献上有所不同。在一个新的体外检测中,证实了这些祖细胞的增殖能力。我们发现,这两个群体都能产生依赖于基质细胞相互作用和 TGF-β调节的类似集落。这些发现为慢性肺部疾病背景下的上皮重塑机制提供了更多的见解,并为开发药物干预以减轻组织重塑提供了希望。