Correlation analysis indicated that serum CX3CL1 in COPD smokers was negatively correlated with FEV<sub>1</sub>/FVC (justified r = -0.319, P < 0.001), FEV<sub>1</sub>/Pre (justified r = -0.476, P < 0.001), FEV<sub>3</sub>/FVC (justified r = -0.354, P < 0.001), MMEF25-75/Pre (justified r = -0.428, P < 0.001), but positively correlated with CRP (justified r = 0.331, P < 0.001) and MMP-12 (justified r = 0.352, P < 0.001).
Serum level of MMP-12 was significantly higher in COPD patients than in controls groups (6.8 ng/ml vs 3.3 ng/ml, respectively; F = 7.433, p < 0.0001), although independently of analyzed gene polymorphisms.
The mRNA expression of MMP-12 (<i>r</i> = -0.3958, <i>P</i> = 0.0186) and NE (<i>r</i> = -0.3694, <i>P</i> = 0.0290) in COPD patients was negatively correlated with pulmonary function.
Matrix metalloproteinase-12 (MMP-12) and Tissue inhibitor of metalloproteinase-4 (TIMP-4) play important roles in the pathophysiology of chronic obstructive pulmonary disease (COPD).
Thus, the basophil-derived IL-4/monocyte-derived IM/MMP-12 axis plays a crucial role in emphysema formation and therefore may be a potential target to slow down emphysema progression at the initiation phase of COPD.
Matrix metalloproteinase-12 (MMP-12, macrophage elastase) is a member of the MMP family that is responsible for the degradation of extracellular matrix, and is associated with the inflammatory process of chronic obstructive pulmonary disease (COPD).
The role of matrix metalloproteinase-12 (MMP-12) in the pathogenesis of several inflammatory diseases such as chronic obstructive pulmonary disease, emphysema, and asthma is well established.
Furthermore, serum levels of neutrophil elastase (NE) and MMP-3 (but not of IL-6 and MMP-12) were also higher in COPD smokers than in healthy smokers before and after adjustment for age and pack-years.
In the current study, we aimed to explore the possible role of MMP12 -82 A > G (rs2276109) promoter polymorphism in the development of COPD in a population from Bulgaria (167 patients with COPD and 119 control individuals).
SERPINE2, FAM13A, and MMP12 associated with higher FEV1 and FVC, and SERPINE2, HHIP, and TGFB1 interacted with cigarette smoke exposure in utero in PIAMA only, showing adverse effects of exposure on FEV1 being limited to children with genotypes conferring the lowest risk of COPD.
We compared the frequency of single nucleotide polymorphisms in genes coding for matrix proteinases (MMP1, MMP2, MMP3, MMP9, MMP12) as well as tissue inhibitor of metalloproteinases (TIMP1) in two groups of subjects: COPD patients (54 subjects) and COPD patients diagnosed for lung cancer occurrence (53 subjects).The levels of the respective proteins in blood serum were also analyzed.
Two are novel associations (top single-nucleotide polymorphism rs379123 in MYO1D and rs9590614 in VMA8) located within genes that function in cell-cell signaling and cell migration, and five are in loci previously associated with chronic obstructive pulmonary disease susceptibility (HHIP, IREB2/CHRNA3, CYP2A6/ADCK, TGFB2, and MMP12).
In this report, we performed Meta analysis to investigate the association between four kinds of MMP single nucleotide polymorphisms (SNP, MMP1 -1607 1G/2G, MMP3 -1171 5A/6A, MMP9 -1562 C/T, MMP12-82 A/G) and COPD risk from 21 studies including 4184 cases and 5716 controls.
This finding supports a role for MMP-12 in the pathogenesis of COPD and might suggest that blocking MMP-12 activity in patients with COPD could prevent the further development of emphysema.
MMP-7 and MMP-12 polymorphisms were genotyped in 85 patients with COPD and 73 healthy control subjects using real-time polymerase chain reaction analysis.
It has previously been shown that individuals homozygous for the A/A allele of rs652438 in MMP-12 are over-represented among patients with severe COPD (n=1517).
To investigate the association of 3 polymorphisms of MMP genes (MMP-1 -1607G-->GG, MMP-9 -1562C-->T and MMP-12N357S), which have been reported to be associated with COPD-related phenotypes, with the risk of COPD in a Korean population.