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dc.contributor.authorXu, Lulu
dc.contributor.authorLu, Yuntao
dc.contributor.authorZhang, Jing
dc.contributor.authorWu, Lian
dc.contributor.authorMerrilees, Mervyn J.
dc.contributor.authorQu, J.
dc.date.accessioned2016-02-26T17:29:39Z
dc.date.available2016-02-26T17:29:39Z
dc.date.issued2015-05-11
dc.identifier.issn1569-9048
dc.identifier.urihttps://hdl.handle.net/10652/3199
dc.description.abstractCOPD lung is characterized by loss of alveolar elastic fibers and an increase in the chondroitin sulfate (CS) matrix proteoglycan versican 1 (V1). V1 is a known inhibitor of elastic fiber deposition and this study investigates the effects of knockdown of V1, and add-back of CS, on CCL-210 lung fibroblasts treated with cigarette smoke extract (CSE) as a model for COPD. CSE inhibited fibroblast proliferation, viability, tropoelastin synthesis, and elastin deposition, and increased V1 synthesis and secretion. V1 siRNA decreased V1 and constituent CS, did not affect tropoelastin production, but blocked the CSE-induced loss in insoluble elastin. Exogenous CS reduced insoluble elastin, even in the presence of V1 siRNA. These findings confirm that V1 and CS impair the assembly of tropoelastin monomers into insoluble fibers, and further demonstrate that specific knockdown of V1 alleviates the impaired assembly of elastin seen in cultures of pulmonary fibroblasts exposed to CSE, indicating a regulatory role for this protein in the pathophysiology of COPD.en_NZ
dc.language.isoenen_NZ
dc.publisherElsevieren_NZ
dc.rightsThis is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.en_NZ
dc.subjectpulmonary fibroblasten_NZ
dc.subjectCOPDen_NZ
dc.subjectelastinen_NZ
dc.subjectversicanen_NZ
dc.subjectchronic obstructive pulmonary disease (COPD)en_NZ
dc.titleKnockdown of versican 1 blocks cigarette-induced loss of insoluble elastin in human lung fibroblastsen_NZ
dc.typeJournal Articleen_NZ
dc.rights.holderElsevieren_NZ
dc.identifier.doidoi:10.1016/j.resp.2015.05.004en_NZ
dc.subject.marsden1116 Medical Physiologyen_NZ
dc.identifier.bibliographicCitationXu, L., Lu, Y., Zhang, J., Wu, L., Merrilees, M., & Qu, J. (2015). Knockdown of versican 1 blocks cigarette-induced loss of insoluble elastin in human lung fibroblasts. Respiratory Physiology & Neurobiology, 2015, pp.1-21. doi:doi:10.1016/j.resp.2015.05.004en_NZ
unitec.institutionFudan University (Shanghai, China)en_NZ
unitec.institutionUnitec Institute of Technologyen_NZ
unitec.institutionUniversity of Aucklanden_NZ
unitec.publication.spage1en_NZ
unitec.publication.lpage21en_NZ
unitec.publication.titleRespiratory Physiology & Neurobiologyen_NZ
unitec.peerreviewedyesen_NZ
dc.contributor.affiliationUnitec Institute of Technologyen_NZ
dc.contributor.affiliationFudan University (Shanghai, China)en_NZ
dc.contributor.affiliationUniversity of Aucklanden_NZ
dc.contributor.affiliationZhongshan Hospital (Shanghai, China)en_NZ
dc.contributor.affiliationRujin Hospital (Shanghai, China)en_NZ
dc.contributor.affiliationHuandong Hospital (Shanghai, China)en_NZ
unitec.identifier.roms57905en_NZ
unitec.institution.studyareaHealth Sciences


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