Deposition of insoluble elastin by pulmonary fibroblasts from patients with COPD is increased by treatment with versican siRNA

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Authors
Wu, Lian
Zhang, Jing
Qu, J.
Bai, C.X.
Merrilees, M.
Author ORCID Profiles (clickable)
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Grantor
Date
2017-01-12
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Type
Journal Article
Ngā Upoko Tukutuku (Māori subject headings)
Keyword
chronic obstructive pulmonary disease (COPD)
pulmonary fibroblast
elastin
versican
COPD
ANZSRC Field of Research Code (2020)
Citation
Wu, L., Zhang, J., Qu, J., Bai, C., & Merrilees, M. (2017). Deposition of insoluble elastin by pulmonary fibroblasts from patients with COPD is increased by treatment with versican siRNA. International Journal of COPD, 12, pp.267-273. doi:10.2147/COPD.S116217
Abstract
A reduced content of alveolar elastic fibers is a key feature of COPD lung. Despite continued elastogenic potential by alveolar fibroblasts in the lung affected by COPD, repair of elastic fibers does not take place, which is due to increased levels of the chondroitin sulfate proteoglycan versican that inhibits the assembly of tropoelastin into fibers. In this study, primary pulmonary fibroblast cell lines from COPD and non-COPD patients were treated with a small interfering RNA (siRNA) against versican to determine if knockdown of versican could restore the deposition of insoluble elastin. Versican siRNA treatment reduced versican expression and secretion by pulmonary fibroblasts from both COPD and non-COPD patients (P<0.01) and significantly increased deposition of insoluble elastin in the COPD cell cultures (P<0.05). The treatment, however, did not significantly affect production of soluble elastin (tropoelastin) in either the COPD or non-COPD cell cultures, supporting a role for versican in inhibiting assembly but not synthesis of tropoelastin. These results suggest that removal or knockdown of versican may be a possible therapeutic strategy for increasing deposition of insoluble elastin and stimulating repair of elastic fibers in COPD lung.
Publisher
Dove Medical Press
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DOI
doi:10.2147/COPD.S116217
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