Pro‐inflammatory phenotype of COPD fibroblasts not compatible with repair in COPD lung

Chronic obstructive pulmonary disease (COPD) is characterized by loss of elastic fibres from small airways and alveolar walls, with the decrease in elastin increasing with disease severity. It is unclear why there is a lack of repair of elastic fibres. We have examined fibroblasts cultured from lung...

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Veröffentlicht in:	Journal of cellular and molecular medicine 2012-07, Vol.16 (7), p.1522-1532
Hauptverfasser:	Zhang, Jing, Wu, Lian, Qu, Jie‐ming, Bai, Chun‐xue, Merrilees, Mervyn J., Black, Peter N.
Format:	Artikel
Sprache:	eng
Schlagworte:	Aged Alveoli Antibodies beta-Galactosidase - genetics beta-Galactosidase - metabolism Cell Proliferation Chronic obstructive pulmonary disease Collagen Cytokines Elastin Emphysema Female Fibers Fibroblasts Fibroblasts - cytology Fibroblasts - metabolism Gene expression Humans Hypotheses Inflammation - genetics Inflammation - physiopathology Interleukin 6 Interleukin 8 Interleukin-6 - genetics Interleukin-6 - metabolism Interleukin-8 - genetics Interleukin-8 - metabolism Interstitial collagenase Lung - physiopathology Lung diseases Lungs Male Matrix metalloproteinase Middle Aged Neutrophils Original Parenchyma Phenotype Phenotypes Prostaglandin E2 Proteins Proteoglycans pro‐inflammatory phenotype Pulmonary Disease, Chronic Obstructive - genetics Pulmonary Disease, Chronic Obstructive - physiopathology pulmonary fibroblasts Real-Time Polymerase Chain Reaction Senescence Tropoelastin Tropoelastin - genetics Tropoelastin - metabolism Up-Regulation Versican Versicans - genetics Versicans - metabolism Wound Healing β-Galactosidase
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