AIM2/IL-1α/TGF-β Axis in PBMCs From Exacerbated Chronic Obstructive Pulmonary Disease (COPD) Patients Is Not Related to COX-2-Dependent Inflammatory Pathway.
Basal expression of COX-2 protein was higher in COPD lung fibroblasts compared to Normal or Smoker fibroblasts but there was no difference in Cox-2 mRNA.
Effect of a single nucleotide polymorphism in miR-146a on COX-2 protein expression and lung function in smokers with chronic obstructive pulmonary disease.
Although COX-2 -765G > C polymorphism was not associated with COPD in either ethnic group, the -765C allele frequency was higher in Chinese than Japanese and haplotype -765G-1195A may confer susceptibility to COPD in Chinese.
After adjustment for age and active smoking, CRP and SAA concentrations were associated with the COX2 polymorphism in controls (p=0.041 and 0.014, respectively) but not in COPD patients.
Cytokines also induced microRNA miR-146a expression in both fibroblasts, but significantly less in COPD fibroblasts. miR-146a caused degradation of COX-2 mRNA; reduced expression prolonged COX-2 mRNA half-life in fibroblasts from subjects with COPD.
After IL-1beta stimulation (1-10 ng/ml) Cox-2 mRNA basal expression increased significantly in controls (from 35 +/- 12 to 94 +/- 4 x10(6) molecules cDNA/microg total RNA, p < 0.01) and in COPD (from 38 +/- 8 to 92 +/- 3, p < 0.01).