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Changes in the number of CD31CD45Sca-1+ cells and Shh signaling pathway involvement in the lungs of mice with emphysema and relevant effects of acute adenovirus infection

Authors Deng MH, Li JH, Gan Y, Chen Y, Chen P

Received 9 December 2016

Accepted for publication 30 January 2017

Published 14 March 2017 Volume 2017:12 Pages 861—872


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Charles Downs

Peer reviewer comments 2

Editor who approved publication: Dr Richard Russell

Minhua Deng,1,2 Jinhua Li,2 Ye Gan,3 Yan Chen,2 Ping Chen2

1Respiratory Medicine Department, PLA Rocket Force General Hospital, Beijing, 2Respiratory Medicine Department, 3Rehabilitation Department, Second Xiangya Hospital, Central South University, Changsha, Hunan Province, People’s Republic of China

COPD is a leading cause of mortality worldwide, and cigarette smoke is a pivotal risk factor. Adenovirus is a common cause of acute exacerbations of COPD and expedites COPD progression. Lung stem/progenitor cells play an important role in the development of COPD, while the relevant mechanism remains elusive. Here, we investigated the number of lung CD31-CD45-Sca-1+ cells and sonic hedgehog (Shh) signaling pathway expression levels in cigarette smoke extract (CSE)-induced emphysema mice, as well as the relevant effects of acute adenovirus infection (AAI).
Materials and methods: BALB/c mice were treated with CSE by intraperitoneal injection and/or adenovirus endotracheal instillation at different time points for 28 days. Lung function, lung histomorphology, CD31-CD45-Sca-1+ cell count, and expression levels of major components in the Shh signaling pathway in the lungs were measured.
Results: CSE intraperitoneal injection and adenovirus endotracheal instillation successfully induced emphysema and AAI in mice, respectively. In the lungs of emphysema mice, both the number of CD31-CD45-Sca-1+ cells and expression levels of Shh signaling pathway molecules were reduced. However, AAI increased the number of inhibited CD31-CD45-Sca-1+ cells and activated the suppression of the Shh signaling pathway.
Conclusion: Both CD31-CD45-Sca-1+ cell numbers and Shh signaling pathway expression levels were downregulated in the lungs of emphysema mice induced by CSE intraperitoneal injection, which likely contributes to the pathogenesis of emphysema. Additionally, these inhibited lung CD31-CD45-Sca-1+ cells and Shh signaling pathway molecules were upregulated during AAI, indicating that they play a protective role in the epithelial repair process after AAI injury.

Keywords: emphysema, stem cells, lung CD31-CD45-Sca-1+ cells, sonic hedgehog signaling pathway, adenovirus

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