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肺稳态和癌症中血管周围肺泡上皮干细胞及其龛的特征。

Characterization of perivascular alveolar epithelial stem cells and their niche in lung homeostasis and cancer.

机构信息

Department of Pharmacology and Regenerative Medicine, University of Illinois College of Medicine, Chicago, IL 60612, USA.

Department of Biomedical Engineering, University of Illinois at Chicago, Chicago, IL 60607, USA.

出版信息

Stem Cell Reports. 2024 Jun 11;19(6):890-905. doi: 10.1016/j.stemcr.2024.04.009. Epub 2024 May 16.

DOI:10.1016/j.stemcr.2024.04.009
PMID:38759645
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11390684/
Abstract

Lung alveolar structure and function are maintained by subsets of alveolar type II stem cells (AT2s), but there is a need for characterization of these subsets and their associated niches. Here, we report a CD44 subpopulation of AT2s characterized by increased expression of genes that regulate immune signaling even during steady-state homeostasis. Disruption of one of these immune regulatory transcription factor STAT1 impaired the stem cell function of AT2s. CD44 cells were preferentially located near macro- blood vessels and a supportive niche constituted by LYVE1 endothelial cells, adventitial fibroblasts, and accumulated hyaluronan. In this microenvironment, CD44 AT2 cells were more responsive to transformation by KRAS than general AT2 cells. Moreover, after bacterial lung injury, there was a significant increase of CD44 AT2s and niche components distributed throughout the lung parenchyma. Taken together, CD44 AT2 cells and their perivascular niche regulate tissue homeostasis and tumor formation.

摘要

肺肺泡结构和功能由肺泡 II 型干细胞（AT2）的亚群维持，但需要对这些亚群及其相关龛进行特征描述。在这里，我们报告了一个 CD44 亚群的 AT2，其特征是调节免疫信号的基因表达增加，即使在稳态稳态期间也是如此。破坏其中一种免疫调节转录因子 STAT1 会损害 AT2 的干细胞功能。CD44 细胞优先位于大血管附近，由 LYVE1 内皮细胞、血管外成纤维细胞和积累的透明质酸组成的支持龛中。在这个微环境中，CD44 AT2 细胞比普通 AT2 细胞对 KRAS 的转化更敏感。此外，在细菌性肺损伤后，CD44 AT2 细胞及其分布在整个肺实质中的龛位成分显著增加。总之，CD44 AT2 细胞及其血管周龛调节组织稳态和肿瘤形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/b009078d7ae1/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/4190e9c511b2/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/8f443de77121/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/f4592fbdeff1/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/fcf53961bad3/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/f45ee39dd361/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/e78e9925ad2c/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/374b06188288/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/b009078d7ae1/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/4190e9c511b2/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/8f443de77121/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/f4592fbdeff1/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/fcf53961bad3/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/f45ee39dd361/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/e78e9925ad2c/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/374b06188288/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2c/11390684/b009078d7ae1/gr7.jpg

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