Enhanced levels of prostaglandin E2 and matrix metalloproteinase-2 correlate with the severity of airflow limitation in stable COPD

Background and objective:  Cyclooxygenase‐2 (COX‐2) and its product prostaglandin E2 (PGE2) have been demonstrated to play critical roles in inflammation in respiratory diseases. However, the role of COX‐2 in airway remodelling in COPD remains to be elucidated. Matrix metalloproteinase‐2 (MMP‐2) is...

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Vydané v:Respirology (Carlton, Vic.) Ročník 13; číslo 7; s. 1014 - 1021
Hlavní autori: CHEN, Yan, CHEN, Ping, HANAOKA, Masayuki, DROMA, Yunden, KUBO, Keishi
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Melbourne, Australia Blackwell Publishing Asia 01.11.2008
Predmet:
airflow limitation
airway remodelling
Airway Resistance - physiology
Asthma - diagnosis
Asthma - metabolism
Asthma - physiopathology
Blotting, Western
COPD
Cyclooxygenase 2 - biosynthesis
cyclooxygenase-2
Dinoprostone - biosynthesis
Enzyme-Linked Immunosorbent Assay
Female
Follow-Up Studies
Forced Expiratory Volume - physiology
Humans
Male
Matrix Metalloproteinase 2 - biosynthesis
matrix metalloproteinase-2
Middle Aged
prostaglandin E2
Severity of Illness Index
Sputum - chemistry
Time Factors
ISSN:1323-7799, 1440-1843, 1440-1843
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Shrnutí:Background and objective:  Cyclooxygenase‐2 (COX‐2) and its product prostaglandin E2 (PGE2) have been demonstrated to play critical roles in inflammation in respiratory diseases. However, the role of COX‐2 in airway remodelling in COPD remains to be elucidated. Matrix metalloproteinase‐2 (MMP‐2) is associated with both inflammation and airway remodelling in COPD. The objective of this study was to measure the expression of COX‐2 and the concentrations of PGE2 and MMP‐2, and to investigate the role of COX‐2 and PGE2 in airflow limitation mediated by MMP‐2, in the pathogenesis of COPD. Methods:  Forty‐three patients with stable COPD, twelve smoking control subjects and ten non‐smoking control subjects were enrolled. Induced sputum was obtained for measurement of the concentrations of PGE2 and MMP‐2 by ELISA. COX‐2 protein expression was assessed by western blotting. Results:  PGE2 and MMP‐2 concentrations were significantly higher in both smoking control subjects and patients with COPD than in non‐smoking control subjects (P < 0.01). Moreover, the levels of PGE2 and MMP‐2 were inversely correlated with FEV1% predicted in COPD patients (PGE2: r = −0.748, P < 0.01; MMP‐2: r = −0.801, P < 0.01). Levels of PGE2 were also positively correlated with those of MMP‐2 in patients with COPD (r = 0.775, P < 0.01). Expression of COX‐2 protein was significantly higher in COPD patients than in non‐smoking control subjects. Conclusions:  COX‐2 and its product PGE2 are not only involved in airway inflammation, but may also contribute to the severity of airflow limitation mediated by MMP‐2 during progression of COPD.
Bibliografia:istex:B0E50D7EA6FCBBB71CA5E35A83515F0473C8518F
ark:/67375/WNG-5D4X7TQ8-N
ArticleID:RESP1365
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1323-7799
1440-1843
1440-1843
DOI:10.1111/j.1440-1843.2008.01365.x