AMs of asthma with a fast FEV<sub>1</sub> decline released a higher level of MMP-9 (8.52 ± 3.53 pg/mL, <i>p</i> < 0.05) than those of a slow FEV<sub>1</sub> decline (0.99 ± 0.20 pg/mL).
In addition, mediators or cytokines, including cysteinyl leukotrienes, matrix metallopeptidase-9, interleukin-33 and eosinophil expression of transforming growth factor-β, may contribute to airway remodeling in asthma.
The increase of oxidative stress and subsequent enhancement of MMP9 and TGF-<i>β</i>1 expression were rescued by the administration of Tetrandrine in the rat model of asthma.
Rutin also inhibited the expression of matrix metalloproteinase 9, thereby aiding in prevention of airway remodelling in asthma thereby revealing to be a potent candidate in asthma therapy.
The aim of this study was to investigate whether variants in 3' end of the MMP9 gene are associated with clinical phenotype and responsiveness to treatment in children with asthma.
Expression levels of ORMDL3, phosphorylated (p)‑ERK and MMP‑9 were significantly greater in the asthma‑model group; however, in the group pretreated with budesonide their expression was reduced.
To investigate whether MMP-9 SNPs are associated with childhood-onset asthma in Mexican patients we conducted a case-control study including 403 children with clinical asthma diagnoses and 426 healthy controls from Mexico.
A water extract of Samchulkunbi-tang attenuates airway inflammation by inhibiting inos and MMP-9 activities in an ovalbumin-induced murine asthma model.
The results showed that the mean serum levels of MMP-9 in the children with asthma (136.53 ± 29.96 ng/ml) were significantly higher than that in the healthy controls (45.08 ± 12.53 ng/ml; P<0.05).
However, the role of the AP-1 sites within the MMP-9 promoter and the effect of commonly used asthma pharmacotherapies in modulating human rhinovirus (HRV)-induced MMP-9 production have not yet been elucidated.
MMP-9 (gelatinase B) is recognized in chronic obstructive pulmonary disease (COPD) and now asthma as playing a central role in matrix degradation in injury, as well as contributing to the remodeling process.
Genotyping of four HapMap derived tagging SNPs in the MMP-9 gene was performed using MALDI-TOF MS in three cross sectional study populations of German children (age 9-11; N = 4,264) phenotyped for asthma and atopic diseases according to ISAAC standard procedures.
Functionally, MMP-9-deficient mice had more acute allergic inflammation than wild-type mice, suggesting that MMP-9 was protective against experimentally induced asthma.
Levels of MMP-9 and TIMP-1 in BAL cell of asthmatic children were increased significantly at about 30- and 35-fold relative to the controls, respectively.