PTGS2 and chronic obstructive pulmonary disease: Our previous study, using primary lung fibroblasts from patients with COPD and smokers without COPD (controls), demonstrated that following stimulation with inflammatory cytokines, fibroblasts from COPD subjects produced higher PGE2 levels relative to those from control subjects, and that elevated PGE2 levels were the result of an increase in COX-2 expression due to alterations in mRNA stability caused by weak induction of microRNA-146a [17].