TY - JOUR
T1 - CTGF upregulation correlates with MMP-9 level in airway remodeling in a murine model of asthma
AU - Lin, Sheng-Chieh
AU - Chou, Hsiu Chu
AU - Chiang, Bor Luen
AU - Chen, Chung Ming
N1 - Funding Information:
This work was supported by the Ministry of Science and Technology (MOST 103-2314-B-038-019-MY3).
Publisher Copyright:
Copyright © 2016 Termedia & Banach.
PY - 2017
Y1 - 2017
N2 - Introduction: Connective tissue growth factor (CTGF) mediates hypertrophy, proliferation, and extracellular matrix synthesis. Matrix metalloproteinase (MMP) plays a role in airway extracellular matrix remodeling. The correlation between CTGF and MMP in airway remodeling of asthma was unknown. This study investigated lung CTGF expression and its correlation with MMP and airway structural changes in a murine model of asthma. Material and methods: Female BALB/c mice were sensitized and challenged by intraperitoneal injections and intranasal phosphate-buffered saline (PBS) or ovalbumin (OVA). Airway responsiveness and serum OVA-specific IgE were measured. Airway structural changes were quantified by morphometric analysis. Differential cell counts and MMP-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-1 were evaluated in bronchoalveolar lavage fluid (BALF). Lung CTGF was determined by Western blot. Results: Serum OVA-specific IgE level and airway responsiveness in enhanced pause (Penh) is significantly higher in sensitized mice challenged with OVA compared to PBS-challenged mice. MMP-2, MMP-9, and TIMP-1 in BALF were significantly higher in OVA mice. Airway structural changes of animals' lungs with OVA challenge showed increased thickness of the smooth muscle layer and numbers of Goblet cells and inflammatory cells and eosinophils near airways and perivascular areas. Lung CTGF expression significantly increased in OVA-challenged mice. CTGF expressions positively correlated with MMP-9 (r = 0.677, p < 0.05), TIMP-1 (r = 0.574, p < 0.05) and thickness of the smooth muscle layer (r = 0.499, p < 0.05). Conclusions: This study indicates that CTGF upregulation correlates with MMP-9, probably involved in the pathogenesis of airway remodeling of asthma.
AB - Introduction: Connective tissue growth factor (CTGF) mediates hypertrophy, proliferation, and extracellular matrix synthesis. Matrix metalloproteinase (MMP) plays a role in airway extracellular matrix remodeling. The correlation between CTGF and MMP in airway remodeling of asthma was unknown. This study investigated lung CTGF expression and its correlation with MMP and airway structural changes in a murine model of asthma. Material and methods: Female BALB/c mice were sensitized and challenged by intraperitoneal injections and intranasal phosphate-buffered saline (PBS) or ovalbumin (OVA). Airway responsiveness and serum OVA-specific IgE were measured. Airway structural changes were quantified by morphometric analysis. Differential cell counts and MMP-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-1 were evaluated in bronchoalveolar lavage fluid (BALF). Lung CTGF was determined by Western blot. Results: Serum OVA-specific IgE level and airway responsiveness in enhanced pause (Penh) is significantly higher in sensitized mice challenged with OVA compared to PBS-challenged mice. MMP-2, MMP-9, and TIMP-1 in BALF were significantly higher in OVA mice. Airway structural changes of animals' lungs with OVA challenge showed increased thickness of the smooth muscle layer and numbers of Goblet cells and inflammatory cells and eosinophils near airways and perivascular areas. Lung CTGF expression significantly increased in OVA-challenged mice. CTGF expressions positively correlated with MMP-9 (r = 0.677, p < 0.05), TIMP-1 (r = 0.574, p < 0.05) and thickness of the smooth muscle layer (r = 0.499, p < 0.05). Conclusions: This study indicates that CTGF upregulation correlates with MMP-9, probably involved in the pathogenesis of airway remodeling of asthma.
KW - Airway remodeling
KW - Asthma
KW - Connective tissue growth factor
KW - Matrix metalloproteinase
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U2 - 10.5114/aoms.2016.60371
DO - 10.5114/aoms.2016.60371
M3 - Article
AN - SCOPUS:85019570092
SN - 1734-1922
VL - 13
SP - 670
EP - 676
JO - Archives of Medical Science
JF - Archives of Medical Science
IS - 3
ER -