Tenascin C in Lung Diseases
by
, and
Chantal Donovan
1,2,†,
Xu Bai
1,3,†,
Yik Lung Chan
1,
Min Feng
1,3,
Kin-Fai Ho
4
,
Hai Guo
5, 
Hui Chen
1
and
Brian G. Oliver
1,3,*
1
School of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, Australia
2
Hunter Medical Research Institute and The University of Newcastle, Newcastle, NSW 2050, Australia
3
Respiratory Cellular and Molecular Biology, Woolcock Institute of Medical Research, Sydney, NSW 2037, Australia
4
Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong SAR 999077, China
5
Air Quality Studies, Department of Civil and Environmental Engineering, Hong Kong Polytechnic University, Hong Kong SAR 999077, China
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Biology 2023, 12(2), 199; https://doi.org/10.3390/biology12020199
Submission received: 16 November 2022
/
Revised: 25 January 2023
/
Accepted: 26 January 2023
/
Published: 28 January 2023
(This article belongs to the Topic Molecular Profiling and Identification of Molecular Signatures Associated with Tissue Development, Tumorigenesis, and Anticancer Agents’ Action)
Simple Summary
Tenascin C (TNC) is an extracellular matrix protein involved in numerous cellular processes in development and can be increased in disease; however, its role in lung diseases is less advanced. In this study, we investigated the expression of TNC during lung development, and in the lungs of offspring following maternal particulate matter (PM) exposure, asthma, chronic obstructive pulmonary disease (COPD), and lung cancer. We found that TNC is increased during lung development, in offspring from PM-exposed dams, and in asthma, COPD, and lung cancer tissues. Therefore, targeting TNC may provide a novel therapeutic target for lung diseases.
Abstract
Tenascin C (TNC) is a multifunctional large extracellular matrix protein involved in numerous cellular processes in embryonic development and can be increased in disease, or under conditions of trauma or cell stress in adults. However, the role of TNC in lung diseases remains unclear. In this study, we investigated the expression of TNC during development, in offspring following maternal particulate matter (PM) exposure, asthma, chronic obstructive pulmonary disease (COPD) and lung cancer. TNC expression is increased during lung development in biopsy cells, endothelial cells, mesenchymal cells, and epithelial cells. Maternal PM exposure increased TNC and collagen deposition, which was not affected by the removal of PM exposure after pregnancy. TNC expression was also increased in basal epithelial cells and fibroblasts in patients with asthma and AT2 and endothelial cells in patients with COPD. Furthermore, there was an increase in the expression of TNC in stage II compared to stage IA lung cancer; however, overall survival analysis showed no correlation between levels of TNC and survival. In conclusion, TNC is increased during lung development, in offspring following maternal PM exposure, and in asthma, COPD, and lung cancer tissues. Therefore, targeting TNC may provide a novel therapeutic target for lung diseases.
Keywords:
lung development; foetal programming; particular matter; asthma; COPD; lung cancer
