Matrix proteins from smoke-exposed fibroblasts are pro-proliferative.

@article{Krimmer2012MatrixPF,
  title={Matrix proteins from smoke-exposed fibroblasts are pro-proliferative.},
  author={David I. Krimmer and Janette Kay Burgess and Teh Kian Wooi and Judith Lee Black and Brian Gregory George Oliver},
  journal={American journal of respiratory cell and molecular biology},
  year={2012},
  volume={46 1},
  pages={
          34-9
        }
}
  • D. Krimmer, J. Burgess, +2 authors B. Oliver
  • Published 14 December 2012
  • Medicine, Biology
  • American journal of respiratory cell and molecular biology
Airway remodeling decreases lung function in chronic obstructive pulmonary disease (COPD). Extracellular matrix (ECM) deposition is increased in remodeled airways and drives cellular processes of proliferation, migration, and inflammation. We investigated the role of cigarette smoke in altering the ECM deposited from human lung fibroblasts. Lung fibroblasts isolated from patients with COPD or other lung disease were exposed to cigarette smoke extract (CSE) and 5 ng/ml transforming growth factor… 
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47 Citations
Background Citations
13
Methods Citations
9
Results Citations
5

47 Citations

Citation Type

Citation Type

Effects of cigarette smoke extract on human airway smooth muscle cells in COPD
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ASM cells from smokers with COPD were more sensitive to CSE stimulation, which may explain, in part, why some smokers develop COPD.
Effects Of Cigarette Smoke Extract On Human Airway Smooth Muscle Cell From COPD
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ASM cells from smokers with COPD were more sensitive to CSE stimulation, which may explain, in part, why some smokers develop COPD.
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Wood Smoke Extract Promotes Extracellular Matrix Remodeling in Normal Human Lung Fibroblasts
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TLDR
A non-neuronal cholinergic system is implicated in cigarette smoke-induced bronchial fibroblast-to-myofibroblast transition, which is inhibited by aclidinium bromide.
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TLDR
The bioactive region/s of fibulin-1C which promotes fibrosis is identified and a useful tool for future studies is described to reveal the mechanisms underlying the pathphysiology of chronic lung diseases.
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