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Enhanced deposition of low-molecular-weight hyaluronan in lungs of cigarette smoke-exposed mice

Ken Bracke UGent, Mieke A Dentener, Eleni Papakonstantinou, Juhanita HJ Vernooy, Tine Demoor, Nele Pauwels UGent, Jack Cleutjens, Robert Jan van Suylen, Guy Joos UGent, Guy Brusselle UGent, et al. (2010) AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY. 42(6). p.753-761
abstract
Chronic obstructive pulmonary disease (COPD) is characterized by infiltration of inflammatory cells, destruction of lung parenchyma, and airway wall remodeling. Hyaluronan (HA) is a component of the extracellular matrix, and low-molecular-weight (LMW) HA fragments have proinflammatory capacities. We evaluated the presence of HA in alveolar and airway walls of C57BL/6 mice that were exposed to air or cigarette smoke (CS) for 4 weeks (subacute) or 24 weeks (chronic). We measured deposition of the extracellular matrix proteins collagen and fibronectin in airway walls and determined the molecular weight of HA purified from lung tissue. In addition, we studied the expression of HA-modulating genes by RT-PCR. HA staining in alveolar walls was significantly enhanced upon chronic CS exposure, whereas HA levels in the airway walls were already significantly higher upon subacute CS exposure and remained elevated upon chronic CS exposure. This differed from the deposition of collagen and fibronectin, which are only elevated at the chronic time point. In lungs of CS-exposed mice, the molecular weight of HA clearly shifted toward more LMW HA fragments. CS exposure significantly increased the mRNA expression of the HA synthase gene Has3 in total lung tissue, whereas the expression of Has! was decreased. These in vivo studies in an experimental model of COPD show that CS exposure leads to enhanced deposition of (mostly LMW) HA in alveolar and bronchial walls by altering the expression of HA-modulating enzymes. This may contribute to airway wall remodeling and pulmonary inflammation in COPD.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
journal title
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
Am. J. Respir. Cell Mol. Biol.
volume
42
issue
6
pages
753 - 761
Web of Science type
Article
Web of Science id
000278671500014
JCR category
RESPIRATORY SYSTEM
JCR impact factor
4.426 (2010)
JCR rank
5/45 (2010)
JCR quartile
1 (2010)
ISSN
1044-1549
DOI
10.1165/rcmb.2008-0424OC
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1193360
handle
http://hdl.handle.net/1854/LU-1193360
date created
2011-03-21 16:49:16
date last changed
2016-12-19 15:45:50
@article{1193360,
  abstract     = {Chronic obstructive pulmonary disease (COPD) is characterized by infiltration of inflammatory cells, destruction of lung parenchyma, and airway wall remodeling. Hyaluronan (HA) is a component of the extracellular matrix, and low-molecular-weight (LMW) HA fragments have proinflammatory capacities. We evaluated the presence of HA in alveolar and airway walls of C57BL/6 mice that were exposed to air or cigarette smoke (CS) for 4 weeks (subacute) or 24 weeks (chronic). We measured deposition of the extracellular matrix proteins collagen and fibronectin in airway walls and determined the molecular weight of HA purified from lung tissue. In addition, we studied the expression of HA-modulating genes by RT-PCR. HA staining in alveolar walls was significantly enhanced upon chronic CS exposure, whereas HA levels in the airway walls were already significantly higher upon subacute CS exposure and remained elevated upon chronic CS exposure. This differed from the deposition of collagen and fibronectin, which are only elevated at the chronic time point. In lungs of CS-exposed mice, the molecular weight of HA clearly shifted toward more LMW HA fragments. CS exposure significantly increased the mRNA expression of the HA synthase gene Has3 in total lung tissue, whereas the expression of Has! was decreased. These in vivo studies in an experimental model of COPD show that CS exposure leads to enhanced deposition of (mostly LMW) HA in alveolar and bronchial walls by altering the expression of HA-modulating enzymes. This may contribute to airway wall remodeling and pulmonary inflammation in COPD.},
  author       = {Bracke, Ken and Dentener, Mieke A and Papakonstantinou, Eleni and Vernooy, Juhanita HJ and Demoor, Tine and Pauwels, Nele and Cleutjens, Jack and van Suylen, Robert Jan and Joos, Guy and Brusselle, Guy and Wouters, Emiel FM},
  issn         = {1044-1549},
  journal      = {AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY},
  language     = {eng},
  number       = {6},
  pages        = {753--761},
  title        = {Enhanced deposition of low-molecular-weight hyaluronan in lungs of cigarette smoke-exposed mice},
  url          = {http://dx.doi.org/10.1165/rcmb.2008-0424OC},
  volume       = {42},
  year         = {2010},
}

Chicago
Bracke, Ken, Mieke A Dentener, Eleni Papakonstantinou, Juhanita HJ Vernooy, Tine Demoor, Nele Pauwels, Jack Cleutjens, et al. 2010. “Enhanced Deposition of Low-molecular-weight Hyaluronan in Lungs of Cigarette Smoke-exposed Mice.” American Journal of Respiratory Cell and Molecular Biology 42 (6): 753–761.
APA
Bracke, Ken, Dentener, M. A., Papakonstantinou, E., Vernooy, J. H., Demoor, T., Pauwels, N., Cleutjens, J., et al. (2010). Enhanced deposition of low-molecular-weight hyaluronan in lungs of cigarette smoke-exposed mice. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 42(6), 753–761.
Vancouver
1.
Bracke K, Dentener MA, Papakonstantinou E, Vernooy JH, Demoor T, Pauwels N, et al. Enhanced deposition of low-molecular-weight hyaluronan in lungs of cigarette smoke-exposed mice. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY. 2010;42(6):753–61.
MLA
Bracke, Ken, Mieke A Dentener, Eleni Papakonstantinou, et al. “Enhanced Deposition of Low-molecular-weight Hyaluronan in Lungs of Cigarette Smoke-exposed Mice.” AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY 42.6 (2010): 753–761. Print.