Reduced miR-146a increases prostaglandin E₂in chronic obstructive pulmonary disease fibroblasts.

ABSTRACT:

Rationale

Persistent inflammation plays a major role in chronic obstructive pulmonary disease (COPD) pathogenesis, but its mechanisms are incompletely defined. Overproduction of the inflammatory mediator prostaglandin (PG) E₂ by COPD fibroblasts contributes to reduced repair function.

Objectives

The present study determined if fibroblasts from subjects with COPD overproduce PGE₂ after stimulation with the inflammatory cytokines IL-1β and tumor necrosis factor-α, and further defined the mechanism for overproduction.

Methods

Fibroblasts were isolated from parenchymal tissue obtained from smokers with and without COPD undergoing lung surgery. PGE₂, cyclooxygenases (COX), and miR-146a in these cells were evaluated by in vitro studies.

Measurements and main results

SUBMITTER: Sato T 

PROVIDER: S-EPMC2970844 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature