scholarly journals 673: Impact of microenvironment on development of lung progenitor cells

2021 ◽  
Vol 20 ◽  
pp. S319
Author(s):  
S. Leir ◽  
J. Kerschner ◽  
S. Yin ◽  
A. Harris
2017 ◽  
Vol 26 (144) ◽  
pp. 170054 ◽  
Author(s):  
Carla F. Kim

The use of stem cell biology approaches to study adult lung progenitor cells and lung cancer has brought a variety of new techniques to the field of lung biology and has elucidated new pathways that may be therapeutic targets in lung cancer. Recent results have begun to identify the ways in which different cell populations interact to regulate progenitor activity, and this has implications for the interventions that are possible in cancer and in a variety of lung diseases. Today's better understanding of the mechanisms that regulate lung progenitor cell self-renewal and differentiation, including understanding how multiple epigenetic factors affect lung injury repair, holds the promise for future better treatments for lung cancer and for optimising the response to therapy in lung cancer. Working between platforms in sophisticated organoid culture techniques, genetically engineered mouse models of injury and cancer, and human cell lines and specimens, lung progenitor cell studies can begin with basic biology, progress to translational research and finally lead to the beginnings of clinical trials.


Author(s):  
Barbara Driscoll ◽  
Alex Kikuchi ◽  
Allison N. Lau ◽  
Jooeun Lee ◽  
Raghava Reddy ◽  
...  

2019 ◽  
Vol 26 (6) ◽  
pp. 1497-1506 ◽  
Author(s):  
Charles Fouillade ◽  
Sandra Curras-Alonso ◽  
Lorena Giuranno ◽  
Eddy Quelennec ◽  
Sophie Heinrich ◽  
...  

2016 ◽  
Vol 6 (3) ◽  
pp. 767-777 ◽  
Author(s):  
Isotta Chimenti ◽  
Francesca Pagano ◽  
Francesco Angelini ◽  
Camilla Siciliano ◽  
Giorgio Mangino ◽  
...  

2020 ◽  
Vol 53 (12) ◽  
Author(s):  
Zixian Zhao ◽  
Yu Zhao ◽  
Yueqing Zhou ◽  
Xiaofan Wang ◽  
Ting Zhang ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1014
Author(s):  
Oliver G. Chen ◽  
Steven E. Mather ◽  
Christian M. Brommel ◽  
Bradley A. Hamilton ◽  
Annie Ehler ◽  
...  

Cystic fibrosis (CF) is caused by genetic mutations of the CF transmembrane conductance regulator (CFTR), leading to disrupted transport of Cl− and bicarbonate and CF lung disease featuring bacterial colonization and chronic infection in conducting airways. CF pigs engineered by mutating CFTR develop lung disease that mimics human CF, and are well-suited for investigating CF lung disease therapeutics. Clinical data suggest small airways play a key role in the early pathogenesis of CF lung disease, but few preclinical studies have focused on small airways. Efficient targeted delivery of CFTR cDNA to small airway epithelium may correct the CFTR defect and prevent lung infections. Adeno-associated virus 4 (AAV4) is a natural AAV serotype and a safe vector with lower immunogenicity than other gene therapy vectors such as adenovirus. Our analysis of AAV natural serotypes using cultured primary pig airway epithelia showed that AAV4 has high tropism for airway epithelia and higher transduction efficiency for small airways compared with large airways. AAV4 mediated the delivery of CFTR, and corrected Cl− transport in cultured primary small airway epithelia from CF pigs. Moreover, AAV4 was superior to all other natural AAV serotypes in transducing ITGα6β4+ pig distal lung progenitor cells. In addition, AAV4 encoding eGFP can infect pig distal lung epithelia in vivo. This study demonstrates AAV4 tropism in small airway progenitor cells, which it efficiently transduces. AAV4 offers a novel tool for mechanistical study of the role of small airway in CF lung pathogenesis in a preclinical large animal model.


Sign in / Sign up

Export Citation Format

Share Document